<?xml version="1.0" encoding="utf-8"?>
			<journal>
			<title>Iranian Journal of Basic Medical Sciences</title>
			<title_fa></title_fa>
			<short_title></short_title>
			<subject>Medical Sciences</subject>
			<web_url>https://ijbms.mums.ac.ir/</web_url>
			<journal_hbi_system_id>0</journal_hbi_system_id>
			<journal_hbi_system_user></journal_hbi_system_user>
			<journal_id_issn>2008-3866</journal_id_issn>
			<journal_id_issn_online>2008-3874</journal_id_issn_online>
			<journal_id_pii></journal_id_pii>
			<journal_id_doi></journal_id_doi>
			<journal_id_iranmedex></journal_id_iranmedex>
			<journal_id_magiran></journal_id_magiran>
			<journal_id_sid></journal_id_sid>
			<journal_id_nlai></journal_id_nlai>
			<journal_id_science></journal_id_science>
			<language>en</language>
			<pubdate>
				<type>jalali</type>
				<year>2026</year>
				<month>11</month>
				<day>1</day>
			</pubdate>
			<pubdate>
				<type>gregorian</type>
				<year>2026</year>
				<month>11</month>
				<day>1</day>
			</pubdate>
			<volume>29</volume>
			<number>11</number>
			<publish_type>online</publish_type>
			<publish_edition>1</publish_edition>
			<article_type>fulltext</article_type>
			<articleset><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Nose-to-brain drug delivery: A new frontier in targeted therapeutics</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Review Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Delivering therapeutics to the Central Nervous System (CNS) remains a major challenge in drug development, largely because the blood–brain barrier (BBB) limits brain exposure for most systemically administered agents. Among alternative delivery routes, intranasal administration has attracted significant interest because it leverages direct anatomical connections between the nasal cavity and the brain, thereby reducing reliance on BBB permeability. This review examines the nasal route, focusing on how olfactory and trigeminal neural pathways contribute to drug transport into the CNS. Rather than assuming a single dominant route, the relative roles of extracellular perineural diffusion, intracellular neuronal transport, perivascular movement, and cerebrospinal fluid–associated distribution are evaluated in light of existing experimental evidence. Key factors that limit or enhance intranasal brain delivery—including mucociliary clearance, local enzymatic activity, drug physicochemical properties, formulation design, and patient-specific variability—are discussed with attention to their practical implications. Recent advances in formulations, such as mucoadhesive and in situ gelling systems, particulate and lipid-based carriers, dendrimers, and stimuli-responsive platforms, are reviewed alongside developments in nasal delivery devices that influence regional deposition.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Brain targeting, Central nervous system targeting, Intranasal, Nanoparticle, Nose-to-brain</keyword>
				<start_page>1617</start_page>
				<end_page>1630</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28438.html</web_url>
			<author_list><author>
				<first_name>SVVS Sai</first_name>
				<middle_name>Sampath</middle_name>
				<last_name>Karakavalasa</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>saisampath2004@gmail.com</email>
				<code>124940</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmaceutical Technology, Raghu College of Pharmacy, Visakhapatnam, Andhra Pradesh, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Rama</first_name>
				<middle_name>Devi</middle_name>
				<last_name>Korni</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ramakalyank@gmail.com</email>
				<code>124939</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmaceutical Technology, Raghu College of Pharmacy, Visakhapatnam, Andhra Pradesh, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Resveratrol as an immune checkpoint inhibitor to enhance the efficacy of breast cancer immunotherapy</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Review Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[A major goal in cancer treatment is to convert “cold” tumors into “hot” ones by altering the tumor microenvironment (TME). Breast cancer is often a cold tumor and is resistant to immunotherapy. Resveratrol is a polyphenolic compound found in grapes, with antioxidant, anti-inflammatory, and potential cardioprotective and anti-aging properties. Resveratrol promotes the conversion of immunologically cold breast tumors into hot tumors, thereby increasing the efficacy of immunotherapy. This article reviews the potential of resveratrol to convert immunologically “cold” breast tumors into “hot” tumors by modulating the TME and enhancing the efficacy of immunotherapy. A comprehensive literature search was conducted in PubMed, Scopus, Web of Science, and Google Scholar to identify English-language articles investigating the effects of resveratrol on immune checkpoints in breast cancer. The results showed that resveratrol suppresses key cancer-promoting pathways (PI3K/Akt/mTOR, MAPK/ERK, STAT/NF-κB, and Wnt/β-catenin) and modulates the immune system. It boosts anti-tumor immunity by activating immunostimulatory cells (such as M1-TAMs, NKs, and CTLs) while simultaneously inhibiting immunosuppressive cells (such as Tregs and MDSCs). It also acts as a natural immune checkpoint inhibitor by targeting the PD-1/PD-L1 pathway. Resveratrol prevents T-cell exhaustion in “cold” tumors and reduces PD-L1 expression in “hot” tumors, thereby enhancing cytotoxic T cells’ ability to attack cancer. However, its effectiveness is limited by poor bioavailability and differences in the biological activity of its metabolites. Future clinical studies are needed to confirm these results and determine optimal therapeutic protocols for resveratrol-mediated breast cancer immunotherapy.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Breast Cancer, Immune cells, Immunotherapy, Natural products, PD-1/PD-L1, Resveratrol, Tumor Microenvironment</keyword>
				<start_page>1631</start_page>
				<end_page>1647</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28244.html</web_url>
			<author_list><author>
				<first_name>Nafiseh Sadat</first_name>
				<middle_name></middle_name>
				<last_name>Alamolhodaei</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>alamolhodaein861@gmail.com</email>
				<code>124186</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmaceutical Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Barry</first_name>
				<middle_name>I.</middle_name>
				<last_name>Hudson</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>barry.hudson@georgetown.edu</email>
				<code>124187</code>
				<coreauthor>No</coreauthor>
				<affiliation>Lombardi Compr 	ehensive Cancer Center, Department of Oncology, Georgetown University Medical Center, Georgetown University, Washington, DC, United States</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Mosaffa</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mosaffaf@mums.ac.ir</email>
				<code>124188</code>
				<coreauthor>No</coreauthor>
				<affiliation>Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Motahareh</first_name>
				<middle_name></middle_name>
				<last_name>Boozari</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>bouzarim@mums.ac.ir</email>
				<code>124189</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmacognosy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Preparation, characterization, and comparison of the release of antibacterial peptide CM11 from PLGA nanoparticles and microparticles</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Pseudomonas aeruginosa (P. aeruginosa) is a Gram-negative bacterium capable of causing acute and chronic infections. Treating these infections is increasingly challenging as this bacterium develops antibiotic resistance. Antimicrobial peptides (AMPs) have emerged as promising therapeutic candidates due to their broad-spectrum activity. Cecropin-Melittin-11 (CM11), a cationic AMP, has shown antimicrobial activity against various pathogens. However, the progression of AMPs from preclinical research to clinical application is hindered by enzymatic degradation, short systemic half-life, and cytotoxicity. To overcome these challenges, poly(lactic-co-glycolic acid)(PLGA) particles for peptide delivery have gained attention.Materials and Methods: CM11-loaded PLGA nanoparticles (NPCM11) and microparticles (MPCM11) were prepared using a double-emulsion solvent evaporation (W1/O/W2) method and characterized for particle size, morphology, encapsulation efficiency, and in vitro release. Their antibacterial activity against planktonic and biofilm-forming P. aeruginosa was evaluated using broth microdilution assay. Their cytocompatibility was evaluated using 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay.Results: Optimum formulations of NPCM11 and MPCM11 were synthesized, exhibiting spherical morphology with average sizes of 281 nm and 7.63 µm, respectively. The encapsulation efficiency (EE%) of NPCM11 and MPCM11 was 63.5% and 60.3%, respectively, while the in vitro CM11 release was 82% and 58%. According to broth microdilution and biofilm inhibition assays, NPCM11 outperformed free CM11 and MPCM11 against planktonic bacteria, whereas both NPCM11 and MPCM11 were superior to free CM11 in biofilm inhibition. MTT assay revealed that NPCM11 and MPCM11 significantly reduced CM11 cytotoxicity. Conclusion: Overall, NPCM11 and MPCM11 were promising formulations of CM11 for treating P. aeruginosa infections.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Antimicrobial peptide, Biofilms, Nanomedicine, Polylactic acid-polyglycolic-acid copolymer, Pseudomonas aeruginosa</keyword>
				<start_page>1648</start_page>
				<end_page>1658</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28429.html</web_url>
			<author_list><author>
				<first_name>Mohammadmahdi</first_name>
				<middle_name></middle_name>
				<last_name>Eshaghi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mohammadeshaghi3782@gmail.com</email>
				<code>124896</code>
				<coreauthor>No</coreauthor>
				<affiliation>Nanobiotechnology Research Center, New Health Technologies Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mehrdad</first_name>
				<middle_name></middle_name>
				<last_name>Moosazadeh Moghaddam</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mm.genetics@gmail.com</email>
				<code>124897</code>
				<coreauthor>No</coreauthor>
				<affiliation>Tissue Engineering and Regenerative Medicine Research Center, New Health Technologies Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Marzieh</first_name>
				<middle_name></middle_name>
				<last_name>Dehghani</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>marziyeh.dehghani@modares.ac.ir</email>
				<code>124898</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biophysics, College of Biological Sciences, Tarbiat Modares University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nematollah</first_name>
				<middle_name></middle_name>
				<last_name>Jonaidi-Jafari</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>jonaidi2000@gmail.com</email>
				<code>124899</code>
				<coreauthor>No</coreauthor>
				<affiliation>Health Management Research Center, Lifestyle and Spiritual Health Research Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hamid</first_name>
				<middle_name></middle_name>
				<last_name>Hesarikia</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>h.hesarikia@gmail.com</email>
				<code>124900</code>
				<coreauthor>No</coreauthor>
				<affiliation>Trauma Research Center, Clinical Sciences Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ramezan Ali</first_name>
				<middle_name></middle_name>
				<last_name>Taheri</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>taheri@bmsu.ac.ir</email>
				<code>124901</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Nanobiotechnology Research Center, New Health Technologies Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Imperatorin alleviates post-infarction cardiac fibrosis via the CD44/PI3K/AKT pathway in mice</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): This study examines the effects of imperatorin (IMP) on cardiac fibrosis in mice with myocardial infarction (MI) and seeks to elucidate the underlying molecular mechanisms.Materials and Methods: C57BL/6 mice were randomly assigned to a control group, an ISO-induced MI group, and ISO+IMP treatment groups (7.5, 15, and 30 mg/kg). 4D-FastDIA-based quantitative proteomics was used for global proteomic analysis to identify differentially expressed proteins (DEPs) and signaling pathways involved in the anti-fibrotic effects of IMP following MI. Echocardiography was performed to evaluate cardiac function; histopathological analysis and serological indicators were used to assess myocardial injury; and Western blotting was employed to verify the expression and mechanisms of related proteins. Results: Compared with the ISO group, IMP treatment markedly improved electrocardiographic abnormalities, reduced serum LDH and cTn-I levels, enhanced cardiac function, and attenuated myocardial injury and fibrosis. Proteomic analysis identified 98 DEPs in the ISO/Control group and 127 DEPs in the ISO+IMP/ISO group. GO and KEGG analyses showed that these DEPs were mainly enriched in fibroblast proliferation-related biological processes and ECM-receptor interaction pathways, with significant involvement of the PI3K/AKT signaling pathway. PPI network analysis highlighted FN1, VTN, Colα2(I), Colα1(III), and CD44 as key regulatory proteins, among which CD44 was notably down-regulated by IMP. Molecular docking demonstrated strong binding affinity between IMP and CD44. Western blot results further confirmed that IMP significantly reduced the expression of fibrosis-related proteins and suppressed activation of the CD44/PI3K/AKT signaling pathway.Conclusion: IMP ameliorates myocardial fibrosis in MI mice by modulating the CD44/PI3K/AKT signaling pathway.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>CD44, Imperatorin, myocardial fibrosis, Myocardial infarction, PI3K/Akt</keyword>
				<start_page>1659</start_page>
				<end_page>1669</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28433.html</web_url>
			<author_list><author>
				<first_name>Hui</first_name>
				<middle_name></middle_name>
				<last_name>Yuan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>huiyuan1982@126.com</email>
				<code>124914</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang 157011, P.R. China|School of Stomatology, Mudanjiang Medical University, Mudanjiang 157011, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>YanKun</first_name>
				<middle_name></middle_name>
				<last_name>Hao</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>466129491@qq.com</email>
				<code>124915</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang 157011, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammed Alaa</first_name>
				<middle_name></middle_name>
				<last_name>Abdulzahra</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mohammed.sadran@uobabylon.edu.iq</email>
				<code>124916</code>
				<coreauthor>No</coreauthor>
				<affiliation>DNA Research Center, University of Babylon, Hilla 51001, Iraq|Department of Pharmacy, AIAmal College for Specialized Medical Sciences, Karbala -56001, Iraq</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>YueYing</first_name>
				<middle_name></middle_name>
				<last_name>Yuan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>yuanyycircle@126.com</email>
				<code>124917</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang 157011, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Xuan</first_name>
				<middle_name></middle_name>
				<last_name>Li</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>1260609327@qq.com</email>
				<code>124918</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang 157011, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Javeria</first_name>
				<middle_name></middle_name>
				<last_name>Qadir</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>javeriaqadir@hotmail.com</email>
				<code>124919</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biological Sciences, International Islamic University Islamabad, Islamabad 04436, Pakistan</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>ManYu</first_name>
				<middle_name></middle_name>
				<last_name>Wang</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>peekaboo8074@163.com</email>
				<code>124920</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang 157011, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>YuanYuan</first_name>
				<middle_name></middle_name>
				<last_name>Zhang</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>1693757090@qq.com</email>
				<code>124921</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang 157011, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>TingTing</first_name>
				<middle_name></middle_name>
				<last_name>Li</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>3062952695@qq.com</email>
				<code>124922</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang 157011, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jian</first_name>
				<middle_name></middle_name>
				<last_name>Sun</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mdjsunjian@126.com</email>
				<code>124923</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Collaborative Innovation Center of Development and Application of North Medicine Resources in Mudanjiang City, Mudanjiang 157011, P.R. China|School of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang 157011, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Acute and chronic zolpidem administration changes hippocampal long-term potentiation (LTP) as a possible mechanism of memory impairment</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Zolpidem is a non-benzodiazepine GABAA receptor positive modulator commonly used to treat short-term insomnia. Given its widespread use, understanding its potential impact on cognitive function and synaptic mechanisms is of great interest. This study aimed to investigate the effects of acute and chronic zolpidem administration on hippocampal long-term potentiation (LTP) as a possible mechanism underlying memory impairment in rats. Materials and Methods: Three groups of rats were used in this study: control, acute (received a single dose of zolpidem, 15 mg/kg), and chronic (received daily doses of zolpidem, 15 mg/kg, for 30 consecutive days). Spatial learning and memory were assessed using the Morris water maze. Basic synaptic transmission and LTP were assessed by recording field excitatory postsynaptic potentials in the hippocampus.Results: No significant differences were observed in spatial learning among the groups. However, evaluation of spatial memory showed that acute and chronic treatment significantly impaired memory performance compared to the control group. Spatial memory was more severely impaired in the chronic group than in the acute group. Electrophysiological data showed that although LTP was induced in both acute and chronic treatment groups, both had significantly lower LTP magnitude than the control group.Conclusion: Chronic zolpidem administration caused significantly greater impairment of spatial memory than acute administration, whereas LTP induction was similarly reduced in both groups. These findings suggest that long-term zolpidem use may pose a greater risk to cognitive function than acute exposure.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Acute, Chronic, Long-term potentiation, Spatial Memory, Zolpidem</keyword>
				<start_page>1670</start_page>
				<end_page>1676</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28436.html</web_url>
			<author_list><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>Rezaeiasl</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>rezaeiasl-z@kaums.ac.ir</email>
				<code>124934</code>
				<coreauthor>No</coreauthor>
				<affiliation>Physiology Research Center, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahmoud</first_name>
				<middle_name></middle_name>
				<last_name>Salami</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>salami-m@kaums.ac.ir</email>
				<code>124935</code>
				<coreauthor>No</coreauthor>
				<affiliation>Physiology Research Center, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hamid</first_name>
				<middle_name>Reza</middle_name>
				<last_name>Banafshe</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>banafshe57@hotmail.com</email>
				<code>124936</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmacology, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran|Department of Addiction Studies, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Modulation of autophagy and PI3K/Akt/mTOR pathway by naringin in sepsis-induced acute kidney injury</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Sepsis-induced acute kidney injury (SI-AKI) is a life-threatening complication with limited treatment options, contributing to high morbidity and mortality worldwide. This study explores the renoprotective effects of naringin (NRG), a bioactive flavonoid, in a rat model of SI-AKI. It hypothesizes that NRG mitigates renal damage by enhancing autophagy and modulating the PI3K/Akt/mTOR pathway, thereby reducing oxidative stress, inflammation, and cellular injury.Materials and Methods: Rats were divided into Control, NRG, LPS, LPS+NRG, and LPS+NRG+3-MA groups. NRG (100 mg/kg) was administered for 14 days, while LPS (10 mg/kg) induced sepsis. The LPS+NRG+3-MA group received 3-MA (30 mg/kg) to inhibit autophagy. Histopathological, immunohistochemical, gene expression, and biochemical analyses were performed. LPS-induced sepsis caused severe renal injury, including inflammation, tubular dilation, and oxidative stress (increased MDA, decreased catalase), alongside elevated TNF-α, NGAL, and KIM-1. Results: NRG treatment significantly preserved renal structure, reduced oxidative stress, and lowered TNF-α, NGAL, and KIM-1 levels. Immunohistochemistry showed increased Beclin-1 and LC3 expression in the LPS+NRG group, suggesting enhanced autophagy. Gene expression analysis revealed activation of the PI3K/Akt/mTOR pathway in NRG-treated rats. Conclusion: These findings indicate that NRG protects against SI-AKI by promoting autophagy and activating pro-survival pathways, offering a novel therapeutic strategy for sepsis management by regulating autophagy and modulating pathways.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Acute kidney injury, Autophagy, Inflammation, Naringin, Sepsis</keyword>
				<start_page>1677</start_page>
				<end_page>1687</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28428.html</web_url>
			<author_list><author>
				<first_name>Ali</first_name>
				<middle_name>Tuğrul</middle_name>
				<last_name>Akin</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>tugrul.akinn@gmail.com</email>
				<code>124884</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Istinye University, Faculty of Medicine, Department of Medical Biology, Istanbul, Turkey|King’s College London, Cancer and Pharmaceutical Sciences, The Rayne Institute, London, UK</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zeynep</first_name>
				<middle_name></middle_name>
				<last_name>Yilmaz</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>zeynep.yilmaz@gmail.com</email>
				<code>124885</code>
				<coreauthor>No</coreauthor>
				<affiliation>Erciyes University, Genome and Stem Cell Center, Kayseri, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Emin</first_name>
				<middle_name></middle_name>
				<last_name>Kaymak</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>e_kaymak@hotmail.com</email>
				<code>124886</code>
				<coreauthor>No</coreauthor>
				<affiliation>Yozgat Bozok University, Faculty of Medicine, Histology-Embryology Department, Yozgat, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Saban</first_name>
				<middle_name></middle_name>
				<last_name>Varinli</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>varinli79@gmail.com</email>
				<code>124887</code>
				<coreauthor>No</coreauthor>
				<affiliation>Yozgat Bozok University, Graduate School of Health Sciences, Histology-Embryology Department, Yozgat, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Esra</first_name>
				<middle_name></middle_name>
				<last_name>Onal</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>esra_onal@gmail.com</email>
				<code>124888</code>
				<coreauthor>No</coreauthor>
				<affiliation>Erciyes University, Graduate School of Health Sciences, Histology-Embryology Department, Kayseri, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Necla</first_name>
				<middle_name></middle_name>
				<last_name>Deger</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>necla_deger38@gmail.com</email>
				<code>124890</code>
				<coreauthor>No</coreauthor>
				<affiliation>Erciyes University, Graduate School of Health Sciences, Histology-Embryology Department, Kayseri, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Meryem</first_name>
				<middle_name></middle_name>
				<last_name>Sayan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sayan.meryem@gmail.com</email>
				<code>124889</code>
				<coreauthor>No</coreauthor>
				<affiliation>Erciyes University, Graduate School of Health Sciences, Histology-Embryology Department, Kayseri, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Derya</first_name>
				<middle_name></middle_name>
				<last_name>Karabulut</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>deryakkus@gmail.com</email>
				<code>124891</code>
				<coreauthor>No</coreauthor>
				<affiliation>Erciyes University, Faculty of Medicine, Histology-Embryology Department, Kayseri, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zuleyha</first_name>
				<middle_name></middle_name>
				<last_name>Doganyigit</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>zuleyha_doganyigit@hotmail.com</email>
				<code>124892</code>
				<coreauthor>No</coreauthor>
				<affiliation>Yozgat Bozok University, Faculty of Medicine, Histology-Embryology Department, Yozgat, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ayse</first_name>
				<middle_name>Tuğrul</middle_name>
				<last_name>Toluk</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>atoluk@erciyes.edu.tr</email>
				<code>124893</code>
				<coreauthor>No</coreauthor>
				<affiliation>Erciyes University, Faculty of Science, Department of Biology, Kayseri, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Protective effects of vitamin B12 against LPS-induced cognitive impairment through modulation of neuroinflammation, oxidative stress, and cholinergic dysfunction</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Neuroinflammation is a key pathological driver of cognitive impairment in neurodegenerative diseases. The endotoxin lipopolysaccharide (LPS) is used to model neuroinflammation, memory impairment, and neurodegeneration. Vitamin B12 has been extensively studied as an anti-oxidant and anti-inflammatory compound that plays an important role in neurological health. The protective effects of vitamin B12 against LPS-induced cognitive impairment, neuroinflammation, oxidative stress, and cholinergic dysfunction were investigated.Materials and Methods: Male Wistar rats were randomly assigned to five groups (n=10 per group): Control, LPS (1 mg/kg, intraperitoneal injection), and three LPS+vitamin B12 (cyanocobalamin) groups receiving 0.25, 0.5, or 1 mg/kg of vitamin B12 by oral gavage. The Morris water maze and passive avoidance tests were conducted, and tissue samples were used to assess oxidative stress, inflammatory markers, and cholinergic activity in the animals’ brains.Results: Vitamin B12 significantly improved memory in the Morris water maze and passive avoidance tests compared with the LPS group (P&lt;0.001), with higher doses being more effective. Vitamin B12 also attenuated oxidative stress and the mRNA expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 (P&lt;0.05-0.001). It also significantly decreased acetylcholinesterase activity (P&lt;0.01-0.001), while the highest dose significantly increased the expression of muscarinic acetylcholine receptor 1 (P&lt;0.01).Conclusion: These findings suggest that B12 may reduce inflammation and oxidative stress, modulate the cholinergic system, and have potential for the prevention and treatment of neuroinflammation and inflammation-induced memory impairment.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Cholinergic system, Learning, Lipopolysaccharides, Memory, Oxidative stress, Vitamin B12</keyword>
				<start_page>1688</start_page>
				<end_page>1698</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28354.html</web_url>
			<author_list><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>Khosravi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>zhrkhosravi76@gmail.com</email>
				<code>124581</code>
				<coreauthor>No</coreauthor>
				<affiliation>Applied Biomedical Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran|Department of Clinical Psychology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Rasul</first_name>
				<middle_name></middle_name>
				<last_name>Saberi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>rasulsaberii@gmail.com</email>
				<code>124582</code>
				<coreauthor>No</coreauthor>
				<affiliation>Applied Biomedical Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran|Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sajjad</first_name>
				<middle_name></middle_name>
				<last_name>Mollaei</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sajjadmollaei98@gmail.com</email>
				<code>124583</code>
				<coreauthor>No</coreauthor>
				<affiliation>Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Elham</first_name>
				<middle_name></middle_name>
				<last_name>Taheri</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>elhamtaheri85@gmail.com</email>
				<code>124584</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Psychology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Afsaneh</first_name>
				<middle_name></middle_name>
				<last_name>Hokmabadi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>hokmabadia1@mums.ac.ir</email>
				<code>124585</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Anatomy and Cell Biology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>Kioumarsi Darbandi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>z.kiumarsi.d@gmail.com</email>
				<code>124586</code>
				<coreauthor>No</coreauthor>
				<affiliation>Applied Biomedical Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran|Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hasan</first_name>
				<middle_name></middle_name>
				<last_name>Hazimeh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>hazimehh981@mums.ac.ir</email>
				<code>124587</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Arezoo</first_name>
				<middle_name></middle_name>
				<last_name>Rajabian</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>rajabianar@mums.ac.ir</email>
				<code>124588</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran|Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahmoud</first_name>
				<middle_name></middle_name>
				<last_name>Hosseini</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>hosseinim@mums.ac.ir</email>
				<code>124589</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Applied Biomedical Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran|Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Sappanone A suppresses CHOP expression and exerts neuroprotective effects in epilepsy</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Sappanone A (SA) is a compound derived from Caesalpinia sappan L that exhibits multiple biological effects, including anti-apoptotic, anti-inflammatory, and anti-oxidant activities. Because oxidative stress, cell apoptosis, and neuroinflammation are associated with the pathophysiology of epilepsy, we conducted this study to explore the role of SA in epilepsy.Materials and Methods: We used SA to treat pentylenetetrazole (PTZ)-induced mice as well as HT22 hippocampal cells exposed to Mg²⁺-free solution. Seizure behavior in the mice was recorded. Nissl staining, TUNEL assay, and flow cytometry were used to evaluate neuronal damage and apoptosis. Moreover, we employed biochemical tests to assess inflammation and oxidative stress levels, and conducted quantitative reverse transcription polymerase chain reaction and western blot to detect CHOP expression.Results: Pretreatments with SA (25 and 50 mg/kg) significantly prolonged seizure latency and reduced seizure duration in PTZ-induced epileptic mice (all P&lt;0.001), whereas 10 mg/kg had no significant effects. At effective doses, SA also alleviated neuronal damage, reduced inflammation, and attenuated oxidative stress (all P&lt;0.05). Furthermore, SA suppressed CHOP expression, and CHOP overexpression partially reversed SA’s protective effects (P&lt;0.05).Conclusion: Our findings suggest that SA pretreatment exerts neuroprotective effects against epilepsy, potentially through suppression of CHOP expression. However, the causal relationship between CHOP suppression and SA-mediated neuroprotection in epilepsy warrants further investigation.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Apoptosis, CHOP, Epilepsy, Inflammation, Oxidative stress, Sappanone A</keyword>
				<start_page>1699</start_page>
				<end_page>1707</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28430.html</web_url>
			<author_list><author>
				<first_name>Jie</first_name>
				<middle_name></middle_name>
				<last_name>Fu</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>fujessie@swmu.edu.cn</email>
				<code>124902</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Neurology, the Affiliated Hospital of Southwest Medical University. Taiping Street, Jiangyang District, Luzhou, 646000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jinglun</first_name>
				<middle_name></middle_name>
				<last_name>Li</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>jinglunli123@163.com</email>
				<code>124903</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurology, the Affiliated Hospital of Southwest Medical University. Taiping Street, Jiangyang District, Luzhou, 646000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Xiu</first_name>
				<middle_name></middle_name>
				<last_name>Chen</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>xiu_chen1@126.com</email>
				<code>124904</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurology, the Affiliated Hospital of Southwest Medical University. Taiping Street, Jiangyang District, Luzhou, 646000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Differential expression of the lncRNA MIR17HG and miR-18a/miR-20a as candidate ncRNA signatures in stage II/III breast cancer and bioinformatic analysis of ncRNA–mRNA regulatory axes</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Breast cancer has remained a significant cause of mortality associated with cancer, necessitating a deeper molecular understanding to improve diagnostics and targeted therapies. Noncoding RNAs (ncRNAs) and their regulatory ncRNA–mRNA axes have recently emerged as important modulators of cancer progression and potential tools for earlier detection and more precise stratification of breast cancer. Among them, MIR17HG variants and the precise regulatory axes of miR-18a/miR-20a, and their mechanisms in stage II/III BC, remain elusive. Materials and Methods: This study addresses this critical gap by integrating data from TCGA miRNAseq and RNAseq datasets with experimental qRT-PCR validation on patient tissues. We investigate MIR17HG transcript variants and their associated miRNAs, especially miR-18a and miR-20a, as candidate stage-associated molecules in stage II/III breast cancer. Co-expressed mRNAs were identified through gene co-expression networks (WGCNA). Results: Potential MIR17HG–miR-18a/20a-mRNA regulatory axes were computationally predicted and functionally annotated to elucidate their involvement in cancer-related signaling pathways. Our findings showed that both MIR17HG splice variants were down-regulated, while their associated miRNAs (miR-18a-5p and miR-20a-5p) were overexpressed. Based on in silico prediction and functional annotation, we propose three candidate MIR17HG-centred axes: MIR17HG–miR-20a–BTG3 (linked to RNA degradation), MIR17HG–miR-18a/miR-20a–PARD6B (Hippo signaling and cell polarity), and MIR17HG–miR-20a–ZNF367 (endocytosis-related processes). Conclusion: Together, these data support MIR17HG and its associated miRNAs as candidate stage II/III breast cancer–associated ncRNA signatures and provide a framework for future functional and clinical validation studies.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Breast Cancer, Endocytosis, Hippo signaling pathway, Long non-coding RNA, MIR17HG, microRNAs, Noncoding RNA, RNA degradation</keyword>
				<start_page>1708</start_page>
				<end_page>1718</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28353.html</web_url>
			<author_list><author>
				<first_name>Reyhane</first_name>
				<middle_name></middle_name>
				<last_name>Alidousti Shahraki</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>reyhanealidousti@modares.ac.ir</email>
				<code>124575</code>
				<coreauthor>No</coreauthor>
				<affiliation>Molecular Genetics Department, Biological Sciences Faculty, Tarbiat Modares University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sara</first_name>
				<middle_name></middle_name>
				<last_name>Tavallaei</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>tavallaei.s@yahoo.com</email>
				<code>124576</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Cell and Molecular Biology &amp; Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Afsaneh</first_name>
				<middle_name></middle_name>
				<last_name>Malekzadeh Shafaroudi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>afsaneh.malekzadeh@um.ac.ir</email>
				<code>124577</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>saba</first_name>
				<middle_name></middle_name>
				<last_name>Abbassioun</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>saba.abbassioun@modares.ac.ir</email>
				<code>124578</code>
				<coreauthor>No</coreauthor>
				<affiliation>Molecular Genetics Department, Biological Sciences Faculty, Tarbiat Modares University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nahid</first_name>
				<middle_name></middle_name>
				<last_name>Nafissi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>nafissi.n@iums.ac.ir</email>
				<code>124579</code>
				<coreauthor>No</coreauthor>
				<affiliation>Rasoul Akram Hospital Clinical Research and Development Center (RCRDC), Iran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seyed-Javad</first_name>
				<middle_name></middle_name>
				<last_name>Mowla</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sjmowla@modares.ac.ir</email>
				<code>124580</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Molecular Genetics Department, Biological Sciences Faculty, Tarbiat Modares University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Britanin alleviates myocardial damage in rats with acute myocardial infarction by inhibiting the JAK2/STAT3 signaling pathway</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Acute myocardial infarction (AMI) is a life-threatening condition featuring coronary occlusion-induced myocardial ischemia-hypoxia, followed by tissue damage driven by calcium overload, inflammation, and pyroptosis. Current therapies offer limited myocardial protection. Britanin, a sesquiterpene lactone from Inula lineariifolia, has anti-inflammatory and antioxidant properties, while its role in AMI remains unclear. This study explored Britanin’s therapeutic effects on rat AMI and underlying mechanisms, focusing on the JAK2/STAT3 signaling pathway.Materials and Methods: Network pharmacology, molecular docking, and ProTox3.0 toxicity prediction were used for target screening and safety evaluation. Rat AMI models were established by left anterior descending ligation and treated with Britanin (5/10 mg/kg). Echocardiography, serum biochemistry, histopathological staining, Western blotting, and qPCR were used to assess cardiac function, myocardial injury, fibrosis, and molecular changes.Results: Pharmacology identified 30 overlapping targets, including JAK2, and highlighted JAK2/STAT3 as a key pathway. Britanin bound JAK2 strongly (binding energy &lt;-8.2 kcal/mol); its LD50 was 150 mg/kg, indicating safety. Britanin improved cardiac function indices, alleviated myocardial fibrosis, reduced serum injury markers, and down-regulated components of the JAK2/STAT3 pathway, the NLRP3 (NOD-like receptor pyrin domain-containing 3) inflammasome, and pyroptosis markers (all P&lt;0.05), without liver or kidney toxicity.Conclusion: Britanin alleviates AMI-induced myocardial damage in rats by improving cardiac function, reducing injury and fibrosis, and inhibiting inflammation and pyroptosis through suppression of the JAK2/STAT3 pathway, positioning it as a potential AMI therapeutic agent.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Acute myocardial infarction, Britanin, JAK2/STAT3 signaling- pathway, NLRP3 inflammasome, Pyroptosis</keyword>
				<start_page>1719</start_page>
				<end_page>1727</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28435.html</web_url>
			<author_list><author>
				<first_name>Yiqing</first_name>
				<middle_name></middle_name>
				<last_name>Zhang</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>zhangyiqing94@outlook.com</email>
				<code>124925</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Medical Center of Soochow University, Suzhou Dushu Lake Hospital, Suzhou City, Jiangsu Province, P. R. China|Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou City, Jiangsu Province, P. R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Xian</first_name>
				<middle_name></middle_name>
				<last_name>Li</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>oliverqueen27@163.com</email>
				<code>124926</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Medical Center of Soochow University, Suzhou Dushu Lake Hospital, Suzhou City, Jiangsu Province, P. R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hezi</first_name>
				<middle_name></middle_name>
				<last_name>Jiang</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>heezjiang@163.com</email>
				<code>124927</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Medical Center of Soochow University, Suzhou Dushu Lake Hospital, Suzhou City, Jiangsu Province, P. R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Guo-Xing</first_name>
				<middle_name></middle_name>
				<last_name>Zhang</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>zhangguoxing@suda.edu.cn</email>
				<code>124924</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Physiology and Neurosciences, Medical College of Soochow University, Suzhou City, Jiangsu Province, P. R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yafeng</first_name>
				<middle_name></middle_name>
				<last_name>Zhou</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>dryafengzhou@163.com</email>
				<code>124928</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Cardiology, The Fourth Affiliated Hospital of Soochow University, Medical Center of Soochow University, Suzhou Dushu Lake Hospital, Suzhou City, Jiangsu Province, P. R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Topical buspirone accelerates wound healing in rats through modulation of inflammation, angiogenesis, and collagen formation</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Cutaneous wound healing is a complex, multistep process that requires coordinated regulation of inflammation, cell proliferation, extracellular matrix deposition, and angiogenesis. This study evaluated the effects of topical buspirone, a partial 5-HT1A receptor agonist, on wound healing in a rat excisional wound model.Materials and Methods: Full-thickness dorsal wounds were created in Wistar rats and treated with topical 0.5% buspirone, 1% phenytoin, vehicle, or left untreated. Wound contraction was assessed macroscopically, and hydroxyproline content, TNF-α, and TGF-β levels were measured to evaluate collagen deposition and inflammatory and fibrotic responses. Histopathological analysis and a chick chorioallantoic membrane (CAM) assay were also performed.Results: Buspirone treatment significantly accelerated wound contraction at all time points compared with the control, vehicle, and phenytoin groups (P&lt;0.001). Hydroxyproline levels were significantly increased, indicating enhanced collagen deposition. In addition, TNF-α levels were reduced, whereas TGF-β levels showed a moderate increase, suggesting balanced modulation of inflammation and fibrosis. Histological findings demonstrated improved re-epithelialization and dermal organization in the buspirone-treated group. Enhanced angiogenesis was also observed in the CAM assay.Conclusion: Overall, topical buspirone may promote wound healing through coordinated effects on inflammation, collagen synthesis, tissue organization, and angiogenesis. This suggests that buspirone is a potential therapeutic agent for wound healing.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>5HT1A, Buspirone, Serotonin receptors, Skin, Wound healing</keyword>
				<start_page>1728</start_page>
				<end_page>1735</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28291.html</web_url>
			<author_list><author>
				<first_name>Mehdi</first_name>
				<middle_name></middle_name>
				<last_name>Zahmatkesh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mahdizahmatkesh1379@gmail.com</email>
				<code>124362</code>
				<coreauthor>No</coreauthor>
				<affiliation>Medicinal Plants and Natural Products Research Center, Institute of Cancer, Hamadan University of Medical Sciences, Hamadan, Iran|Department of Pharmacology and Toxicology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Pari</first_name>
				<middle_name></middle_name>
				<last_name>Tamri</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ptamri@gmail.com</email>
				<code>124363</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Medicinal Plants and Natural Products Research Center, Institute of Cancer, Hamadan University of Medical Sciences, Hamadan, Iran|Department of Pharmacology and Toxicology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mojdeh</first_name>
				<middle_name></middle_name>
				<last_name>Mohammadi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>m.mohammadi@umsha.ac.ir</email>
				<code>124364</code>
				<coreauthor>No</coreauthor>
				<affiliation>Medicinal Plants and Natural Products Research Center, Institute of Cancer, Hamadan University of Medical Sciences, Hamadan, Iran|Department of Pharmacology and Toxicology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Mirzaei</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>fatemehmirzaei1990@gmail.com</email>
				<code>124365</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Anatomical Sciences, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Harmaline improves diabetes-associated renal alterations in nicotinamide/streptozotocin-induced diabetic mice: Possible involvement of oxidative stress, inflammation, and renin–angiotensin system signaling</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Diabetic nephropathy (DN) is marked by structural and functional kidney damage, driven by oxidative stress, inflammation, and renin–angiotensin system (RAS) dysregulation. Harmaline (HAR), a β-carboline alkaloid with potent antioxidant and anti-inflammatory properties, is a promising multi-target therapeutic candidate.Materials and Methods: Twenty-four male mice were randomized into vehicle control (CO), diabetic (DI; nicotinamide 120 mg/kg+streptozotocin 65 mg/kg), diabetic treated with HAR (DI/HAR; 30 mg/kg), or diabetic treated with metformin (DI/MET; 150 mg/kg). After ten days, renal tissues and blood were analyzed for oxidative stress, inflammatory and RAS markers, microRNA expression, and histopathological alterations.Results: Harmaline reversed the changes in total oxidant status and malondialdehyde levels in kidney tissue of diabetic mice. Histopathological analysis showed significant improvement in kidney injury in diabetic mice receiving harmaline. Harmaline treatment decreased the expression of miR-125b, nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). Also, in the antioxidant pathway, there was an increase in the levels of miR-200a, nuclear factor erythroid-related2 (Nrf2), and NAD(P)H quinone dehydrogenase 1 (Nqo1), and a decrease in ECH-like chelate-associated protein1 (Keap1) in kidney tissue. This treatment also decreased the expression of angiotensin-converting enzyme 1 (ACE1) and angiotensin II receptor 1 (AT1R), as well as angiotensin II levels. Conclusion: Harmaline confers renoprotection in experimental DN by simultaneously regulating oxidative stress, inflammatory signaling, and RAS pathways, supporting its potential as a multi-target therapeutic strategy. This study highlights HAR as a promising candidate for translational intervention in diabetic kidney disease.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Diabetic nephropathy, Harmaline, Inflammation, microRNAs, NF-kappa B, Nuclear factor E2-related factor 2, Oxidative stress</keyword>
				<start_page>1736</start_page>
				<end_page>1746</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28450.html</web_url>
			<author_list><author>
				<first_name>Farima</first_name>
				<middle_name></middle_name>
				<last_name>Malekinia</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>farimamalekiania74074@gmail.com</email>
				<code>124991</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Akram</first_name>
				<middle_name></middle_name>
				<last_name>Ahangarpour</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ahangarpur@ajums.ac.ir</email>
				<code>124992</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Diabetes Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Khojasteh</first_name>
				<middle_name></middle_name>
				<last_name>Hoseinynejad</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>khoseinynejad@yahoo.com</email>
				<code>124993</code>
				<coreauthor>No</coreauthor>
				<affiliation>Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seyyed Ali</first_name>
				<middle_name></middle_name>
				<last_name>Mard</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>alimard77@gmail.com</email>
				<code>124994</code>
				<coreauthor>No</coreauthor>
				<affiliation>Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Maryam</first_name>
				<middle_name></middle_name>
				<last_name>Radan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>radan.maryam@yahoo.com</email>
				<code>124995</code>
				<coreauthor>No</coreauthor>
				<affiliation>Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fereshteh</first_name>
				<middle_name></middle_name>
				<last_name>Nejaddehbashi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>fereshte_negad@yahoo.com</email>
				<code>124996</code>
				<coreauthor>No</coreauthor>
				<affiliation>Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Enhanced effects of Wharton’s jelly–derived MSC secretome and microbial exopolysaccharide on cellular responses and tissue repair in diabetic wound healing</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Diabetic wounds are characterized by impaired healing and chronic inflammation. This study evaluated a combination therapy using an exopolysaccharide derived from Rhodotorula mucilaginosa sp. GUMS16 (EPS-GUMS16) and Wharton’s jelly-derived mesenchymal stem cell-conditioned medium (WCM) to accelerate wound repair.Materials and Methods: Human foreskin fibroblasts (HFFs) and human umbilical vein endothelial cells (HUVECs) were treated with an optimized concentration of the WCM/EPS-GUMS16 (WCM/EPS) combination. In vitro assays, including MTT and scratch wound assays, were conducted to assess cell proliferation and migration. In vivo, full-thickness wounds in diabetic rats were treated with WCM/EPS via subcutaneous injection and topical application. Wound healing was monitored by measuring the reduction in wound surface area, and histopathological evaluation was performed using hematoxylin and eosin (H&amp;E) and Masson’s trichrome (MT) staining.Results: In vitro assessments showed that WCM/EPS enhanced fibroblast proliferation and migration (P&lt;0.05) and significantly upregulated CDK-4 expression (P&lt;0.05). In vivo, treated wounds exhibited increased epidermal thickness and altered blood vessel density compared with controls. Semi-quantitative histopathological analysis further revealed enhanced re-epithelialization, more organized granulation tissue, and reduced inflammation and edema. These findings indicate that WCM/EPS effectively modulates inflammation and angiogenesis, thereby promoting tissue regeneration in diabetic wounds.Conclusion: Overall, this combination is a promising strategy for improving diabetic wound healing and highlights the potential of integrating microbial exopolysaccharides with stem cell-derived conditioned media in regenerative therapies.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Diabetes Mellitus, Wound healing, Mesenchymal stem cells, Secretome, Fibroblasts, Endothelial cells, Exopolysaccharide</keyword>
				<start_page>1747</start_page>
				<end_page>1758</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28293.html</web_url>
			<author_list><author>
				<first_name>Hossein</first_name>
				<middle_name></middle_name>
				<last_name>Rostami</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>h_rostami@razi.tums.ac.ir</email>
				<code>124377</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Applied Cell Sciences, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seyed Mohamad Amin</first_name>
				<middle_name></middle_name>
				<last_name>Haramshahi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sma.haramshahi@gmail.com</email>
				<code>124378</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Tissue Engineering and Regenerative Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran|Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nasim</first_name>
				<middle_name></middle_name>
				<last_name>Vousooghi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>dr.n.vosoughi@gmail.com</email>
				<code>124379</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Applied Cell Sciences, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Somayeh</first_name>
				<middle_name></middle_name>
				<last_name>Shamlou</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>somayeh.shamlou@gmail.com</email>
				<code>124380</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Applied Cell Sciences, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zeinab</first_name>
				<middle_name></middle_name>
				<last_name>Shahmahmoudi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>z.shahmahmoodi@gmail.com</email>
				<code>124381</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Tissue Engineering and Regenerative Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran|Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Peiman</first_name>
				<middle_name>Brouki</middle_name>
				<last_name>Milan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>peiman.brouki@gmail.com</email>
				<code>124382</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Tissue Engineering and Regenerative Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran|Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Javad</first_name>
				<middle_name></middle_name>
				<last_name>Verdi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>j-verdi@sina.tums.ac.ir</email>
				<code>124383</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Applied Cell Sciences, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Rutin attenuates cuprizone-induced demyelination in C57BL/6 mice through activation of Nrf2 signaling and inhibition of NF-κB</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Multiple sclerosis (MS) is a debilitating demyelinating disease characterized by oxidative stress and neuroinflammation. This study investigated the therapeutic potential of rutin, a natural flavonoid, in a cuprizone (CPZ)-induced mouse model of demyelination. Materials and Methods: Male C57BL/6 mice were fed a 0.2% CPZ diet for six weeks to induce central nervous system demyelination and were concurrently treated with rutin (50 or 100 mg/kg, intraperitoneally, for the last 14 days). Behavioral assessments, histochemical examinations, and immunohistochemistry for Nrf2, HO-1, NQO-1, and NF-kB p65 were then performed. Results: Behavioral tests revealed that rutin dose-dependently improved CPZ-induced motor coordination deficits in the pole, rotarod, and open-field tests. Histological analysis (LFB and H&amp;E staining) demonstrated that rutin significantly attenuated demyelination in the corpus callosum. Mechanistically, immunohistochemistry showed that rutin treatment effectively up-regulated the key antioxidant pathway by increasing the expression of phosphorylated Nrf2 (p-Nrf2) and its downstream targets (HO-1 and NQO-1), while simultaneously suppressing the pro-inflammatory NF-κB p65 pathway.Conclusion: Our findings show that rutin protects against demyelination through a dual mechanism of enhancing endogenous antioxidant defenses and inhibiting neuroinflammation, highlighting it as a promising candidate for further studies on demyelinating disorders such as MS.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Cuprizone, Demyelination, Mice, NF-kB, Nrf2, Rutin</keyword>
				<start_page>1759</start_page>
				<end_page>1768</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28452.html</web_url>
			<author_list><author>
				<first_name>Seyede Darya</first_name>
				<middle_name></middle_name>
				<last_name>Alavi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>alavi_darya@yahoo.com</email>
				<code>125000</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee, Faculty of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Samira</first_name>
				<middle_name></middle_name>
				<last_name>Shirooie</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>shirooie@gmail.com</email>
				<code>125001</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Antoni</first_name>
				<middle_name></middle_name>
				<last_name>Sureda</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>tosugo@hotmail.com</email>
				<code>125002</code>
				<coreauthor>No</coreauthor>
				<affiliation>Research Group on Community Nutrition and Oxidative Stress (NUCOX) and Health Research Institute of Balearic Islands (IdISBa), University of Balearic Islands-IUNICS, Palma de MallorcaE-07122, Balearic Islands, Spain|CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), 28029 Madrid, Spain</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad Hosein</first_name>
				<middle_name></middle_name>
				<last_name>Farzaei</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mh.farzaei@gmail.com</email>
				<code>125003</code>
				<coreauthor>No</coreauthor>
				<affiliation>Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sajad</first_name>
				<middle_name></middle_name>
				<last_name>Fakhri</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>pharmacy.sajad@yahoo.com</email>
				<code>125004</code>
				<coreauthor>No</coreauthor>
				<affiliation>Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sedigheh</first_name>
				<middle_name></middle_name>
				<last_name>Asgary</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mahtabkeshvari87@gmail.com</email>
				<code>125030</code>
				<coreauthor>No</coreauthor>
				<affiliation>Isfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Linalool restores post-morphine hippocampal-striatal PI3K/Akt and CREB/ΔFosB mRNA expression and LFP power in adult male rats</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Opioid use disorder (OUD) is a chronic, relapsing condition characterized by compulsive drug seeking and profound abstinence-related disturbances. Opioid receptors are distributed across reward-related regions, including the ventral tegmental area (VTA), the ventral striatum (VS), and the hippocampus. Key mediators—PI3K-Akt in the hippocampus and CREB/ΔFosB in the striatum—modulate opioid addiction along the hippocampal–VS axis.Materials and Methods: Rats underwent conditioned place preference (CPP) with three phases: pre-conditioning, conditioning, and post-conditioning. During conditioning, animals received morphine (10 mg/kg, IP) for three days, with or without linalool (50 mg/kg, IP, 30 min prior to morphine). This three-day protocol models reward learning rather than chronic dependence. Groups: saline, morphine, and morphine+linalool. Behavioral tests assessed CPP score, passive avoidance memory, anxiety- and depression-like behaviors, and locomotion. Molecular analyses measured PI3K and Akt mRNA expression (real-time PCR) in the hippocampus and CREB/ΔFosB in the VS. Local field potentials (LFPs) were recorded directly from the hippocampal CA1 and the nucleus accumbens (NAc, part of the VS) via implanted electrodes.Results: Linalool significantly attenuated morphine-induced CPP, improved passive avoidance memory, and reduced anxiety/depressive-like behaviors. Linalool decreased morphine-induced up-regulation of CREB/ΔFosB in VS and PI3K/Akt mRNA in the hippocampus. LFP power in CA1 and NAc was reduced by morphine and restored by linalool.Conclusion: Linalool attenuates morphine-induced reward, memory deficits, and affective disturbances, which are key features of opioid abstinence-induced behavioral disturbances, and normalizes molecular and electrophysiological alterations in the hippocampal-striatal circuit. Although direct causality is not established, linalool is a promising natural compound for managing opioid-associated behavioral disturbances.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>&amp;Delta, FosB, Hippocampus, LFP, Linalool, Morphine, PI3K, Ventral striatum</keyword>
				<start_page>1769</start_page>
				<end_page>1778</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_28197.html</web_url>
			<author_list><author>
				<first_name>Mohsen</first_name>
				<middle_name></middle_name>
				<last_name>Khanlari Piraliloo</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>khanlari.m@gmail.com</email>
				<code>123972</code>
				<coreauthor>No</coreauthor>
				<affiliation>Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yaghoob</first_name>
				<middle_name></middle_name>
				<last_name>Farbood</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>farbood.y@gmail.com</email>
				<code>123973</code>
				<coreauthor>No</coreauthor>
				<affiliation>Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Alireza</first_name>
				<middle_name></middle_name>
				<last_name>Sarkaki</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sarkaki.a@gmail.com</email>
				<code>123974</code>
				<coreauthor>No</coreauthor>
				<affiliation>Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Neda</first_name>
				<middle_name></middle_name>
				<last_name>Yazdanfar</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>yazdanfar.n@gmail.com</email>
				<code>123975</code>
				<coreauthor>No</coreauthor>
				<affiliation>Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seyedeh Parisa</first_name>
				<middle_name></middle_name>
				<last_name>Navabi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>navabi.p@gmail.com</email>
				<code>123976</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article>
			</articleset>
			</journal>