<?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>4</month>
				<day>1</day>
			</pubdate>
			<pubdate>
				<type>gregorian</type>
				<year>2026</year>
				<month>4</month>
				<day>1</day>
			</pubdate>
			<volume>29</volume>
			<number>4</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>Phenotypic alterations in the immune system and tolerance induction in tumor-draining lymph nodes</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[The cause of 90% of all cancer-related fatalities is metastasis. There are two main pathways for the spread of cancer cells: the blood and lymphatic systems. The underlying mechanism of lymphatic metastasis has been well established. However, our understanding of the molecular basis of lymphatic metastasis is still incomplete. Conceptually, cancer cells invade lymphatic vessels (LVs), passively disseminate towards lymphatic nodes, migrate to sentinel lymphatic nodes (SLNs; the first LNs to which cancer cells spread from the primary tumor), and then enter the bloodstream. Before arrival, cancer cells release specific soluble factors that modulate the SLN microenvironment, creating an immunosuppressive environment. After colonization, cancer cells suppress anti-tumor immunity by stimulating regulatory T cells, inhibiting dendritic cell and CD8+ T cell function, and promoting the release of immunosuppressive cytokines. SLNs serve as a microanatomical site for metastasis and play a crucial role in immune modulation. Developing new strategies to reverse tumor-induced remodeling of SLNs may reactivate immunity and reduce accumulation and metastasis. This review discusses the immunological changes induced by tumors in tumor-draining LNs (TDLNs). We also explore their reciprocal relationship and their impact on metastasis and LN immunity, demonstrating how a proper understanding of events occurring in TDLNs can create new opportunities for cancer immunotherapy.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Cellular reprogramming, Immune tolerance, Neoplasm metastasis, Sentinel lymph nodes, Tumor Microenvironment</keyword>
				<start_page>488</start_page>
				<end_page>497</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27359.html</web_url>
			<author_list><author>
				<first_name>Zohreh</first_name>
				<middle_name></middle_name>
				<last_name>Koohini</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.koohini@gmail.com</email>
				<code>120155</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mansoureh</first_name>
				<middle_name></middle_name>
				<last_name>Karimi Kakh</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.kk1992@yahoo.com</email>
				<code>120156</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zeinab</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>rajabianzeinab@yahoo.com</email>
				<code>120157</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Immunology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>Koohini</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>zozohi1212@gmail.com</email>
				<code>120158</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Genetics, School of Medicine, Iran 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>Ultrasound medicine in the era of precision theranostics: Mechanisms, molecular strategies, and clinical translation</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[Ultrasound (US) has evolved from a solely diagnostic tool into a multifaceted theranostics platform, proficient in both high-resolution imaging and tailored therapeutic intervention. Progress in acoustic physics, microbubble and nanobubble technology, and precision beam-forming has broadened its applications in cancer, neurology, cardiovascular diseases, and regenerative medicine. Notwithstanding these advancements, the translation into conventional clinical procedures is impeded by inadequate mapping of acoustic thresholds, variable safety factors, and insufficient integration with molecular and immunological targeting techniques, such as limited ligand specificity, off-target effects, and inconsistent activation of immune responses. This study consolidates the present knowledge of the mechanical, thermal, and sonochemical processes involved in US tissue interactions, focusing on controlled cavitation, bioheat transfer, and the formation of reactive oxygen species. We investigate novel molecular techniques, such as ultrasound-targeted drug delivery, gene therapy, immunomodulation, and sonodynamic treatment, emphasizing significant preclinical and clinical achievements. The exploration of cross-modality synergies, including magnetic resonance imaging, photoacoustic imaging, and nuclear medicine, demonstrates how US might enhance current diagnostic and therapeutic processes. Particular emphasis is centered on the tumor microenvironment, where US may influence immune cell migration, destroy stromal barriers, and augment the effectiveness of checkpoint inhibitors. In regenerative medicine, low-intensity pulsed ultrasound (LIPUS) is assessed for its function in mechanotransduction and tissue healing.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>High-intensity focused-ultrasound, Low-intensity pulsed-ultrasound, Molecular imaging, Sonoporation, Theranostics, Ultrasound</keyword>
				<start_page>498</start_page>
				<end_page>521</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27392.html</web_url>
			<author_list><author>
				<first_name>Lei</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>wanglei198573@163.com</email>
				<code>120330</code>
				<coreauthor>No</coreauthor>
				<affiliation>Affiliated Hospital of Jinggangshan University, Ji’an Jiangxi, 343000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zhiyu</first_name>
				<middle_name></middle_name>
				<last_name>Luo</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>zhiyu.luo1200@gmail.com</email>
				<code>120331</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Affiliated Hospital of Jinggangshan University, Ji’an Jiangxi, 343000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Dan</first_name>
				<middle_name></middle_name>
				<last_name>Liu</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>liudan198192@163.com</email>
				<code>120332</code>
				<coreauthor>No</coreauthor>
				<affiliation>Jinggangshan University, Ji’an Jiangxi, 343009, 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>Cannabidiol: Pharmaceutical formulations and biomedical applications</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[Cannabidiol (CBD) is a phytocannabinoid compound that can be utilized in different pharmaceutical industries. However, high lipophilicity and extensive first-pass metabolism limit its further applications. Therefore, the development of delivery approaches to overcome these obstacles has been of great interest. Herein, a comprehensive review of CBD, the receptors it targets, pharmacokinetic studies, and pharmaceutical formulations for effective delivery is presented. A comprehensive search was conducted in the Scopus, Web of Science, PubMed, and Google Scholar databases from 2016 to 2025. Different in vitro, in vivo, and clinical studies were included, whereas dissertations and conference abstracts were excluded.The results showed that CBD can target 5-HT1A, TRPV1-4, and PPAR-γ with minimal CB1/CB2 agonistic effects. This is consistent with the fact that CBD is effective in the treatment of epilepsy, pain, inflammation, neuropsychiatric disorders, and cancer without expressing psychoactive effects. Additionally, it was indicated that oral delivery formulations, such as long-chain triglyceride vehicles, self-nanoemulsifying systems, and polymeric/microencapsulated carriers, can improve CBD solubility and accelerate its absorption. Pulmonary delivery provides rapid absorption and is suitable for rapid symptom control, whereas intranasal formulations are suitable for nose-to-brain delivery. Transdermal systems elicit localized anti-inflammatory and neuroprotective effects, whereas transmucosal systems can bypass first-pass metabolism. CBD shows promising therapeutic potential; however, its effects across organs depend primarily on the route of administration. All formulations can be effective, but long-term safety evaluations are necessary.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Cannabidiol, Cannabis sativa, Intranasal delivery, Nanotechnology, Oral delivery, Pulmonary delivery, Transmucosal delivery</keyword>
				<start_page>522</start_page>
				<end_page>530</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27439.html</web_url>
			<author_list><author>
				<first_name>Ali</first_name>
				<middle_name></middle_name>
				<last_name>Fadavi Eslam</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>ali_fadavieslam@yahoo.com</email>
				<code>120510</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacognosy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Leila</first_name>
				<middle_name></middle_name>
				<last_name>Mohtashami</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>mohtashamil@mums.ac.ir</email>
				<code>120511</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacognosy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Parvin</first_name>
				<middle_name></middle_name>
				<last_name>Moghimi</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>parvinmoghimi68@gmail.com</email>
				<code>120512</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>Mehrdad</first_name>
				<middle_name></middle_name>
				<last_name>Iranshahi</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>iranshahim@mums.ac.ir</email>
				<code>120513</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Biotechnology Research Center, Pharmaceutical Technology Institute, 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>Targeting amyloid-β in Alzheimer’s disease: A critical analysis of clinical trials and their implications for drug development</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[Alzheimer’s disease (AD), a prevalent neurodegenerative dementia, is characterized by amyloid-β (Aβ) plaques and neurofibrillary tangles, with Aβ playing a central pathogenic role. Approved AD drugs, primarily acetylcholinesterase inhibitors, only alleviate symptoms without modifying disease progression. Aβ-targeting strategies aim to inhibit Aβ production or enhance its clearance, leveraging early deposition for proactive intervention. Preclinical studies show Aβ reduction mitigates neurodegeneration, but clinical trials reveal challenges: γ-secretase inhibitors face off-target toxicities and limited efficacy, while BACE1 inhibitors suffer from safety issues or failure to improve cognition. Despite setbacks, advancing understanding of AD pathogenesis and optimized drug design/ trial protocols sustain the potential of Aβ-targeted therapies. This review aims to advance Aβ-targeted therapies for AD by integrating lessons from prior clinical trials and outlining strategic directions for future research and development. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>γ-Secretase, Aβ, Alzheimer’s disease, APP, BACE1, Small-molecule drugs</keyword>
				<start_page>531</start_page>
				<end_page>543</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27372.html</web_url>
			<author_list><author>
				<first_name>Mengyu</first_name>
				<middle_name></middle_name>
				<last_name>Han</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>13665675695@163.com</email>
				<code>120219</code>
				<coreauthor>No</coreauthor>
				<affiliation>Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, 450046, Henan province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zhonghua</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>lizh@hactcm.edu.cn</email>
				<code>120220</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, 450046, Henan province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Tiancheng</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>18337897180@163.com</email>
				<code>120221</code>
				<coreauthor>No</coreauthor>
				<affiliation>Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, 450046, Henan province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Bingyu</first_name>
				<middle_name></middle_name>
				<last_name>Xiao</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>15515677282@163.com</email>
				<code>120222</code>
				<coreauthor>No</coreauthor>
				<affiliation>Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, 450046, Henan province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jiaxin</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>m17838807176@163.com</email>
				<code>120223</code>
				<coreauthor>No</coreauthor>
				<affiliation>Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, 450046, Henan province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sijia</first_name>
				<middle_name></middle_name>
				<last_name>Liu</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>15836772615@163.com</email>
				<code>120224</code>
				<coreauthor>No</coreauthor>
				<affiliation>Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, 450046, Henan province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jige</first_name>
				<middle_name></middle_name>
				<last_name>Yang</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>y15638418801@163.com</email>
				<code>120225</code>
				<coreauthor>No</coreauthor>
				<affiliation>Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, 450046, Henan province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jinlian</first_name>
				<middle_name></middle_name>
				<last_name>Ma</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>lianzi556@163.com</email>
				<code>120226</code>
				<coreauthor>No</coreauthor>
				<affiliation>Collaborative Innovation Center of Prevention and Treatment of Major Diseases by Chinese and Western Medicine, Henan University of Chinese Medicine, Zhengzhou, 450046, Henan Province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Pan</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>w.p1008@hotmail.com</email>
				<code>120227</code>
				<coreauthor>No</coreauthor>
				<affiliation>Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, 450046, Henan province, China|Collaborative Innovation Center of Prevention and Treatment of Major Diseases by Chinese and Western Medicine, Henan University of Chinese Medicine, Zhengzhou, 450046, Henan Province, 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>Characterization of exosomes from hypoxia-activated human amniotic membrane mesenchymal stem cells</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): Hypoxia is a physical stimulus that enhances stem cell activities to produce more cellular derivatives, particularly exosomes. Enhancing the quantity and quality of exosomes can improve their therapeutic properties. The study aimed to evaluate the effects of normoxic (22%O2) and hypoxic (1%O2) conditions on the characteristics of amniotic membrane-derived mesenchymal stem cells (AM-MSCs) and their exosomes.Materials and Methods: AM-MSCs were isolated, confirmed, and cultured under normoxic and hypoxic conditions. Exosomes were extracted from AM-MSCs and assessed for morphological characteristics (size/distribution/surface topography), structural properties (aggregation/colloidal particle behavior/surface charge/stability), chemical features (functional groups/ionic interactions), biological capacities (total protein concentration), and biocompatibility (microbiological quality/cytotoxicity/irritation/sensitization). Results: Hypoxia did not adversely affect the stemness potential of AM-MSCs (P&gt;0.05). The average sizes of exosomes derived from AM-MSCs (AM-MSCs-Exo) were 185.7±23 nm (PI=0.756) and 145.4±36 nm (PI=0.420) under normoxic and hypoxic conditions, respectively (P≤0.05). Zeta potential of AM-MSCs-Exo was -12.57±0.5 mV under normoxia, while it was -2.37±0.73 mV in the hypoxic conditions. Exosomes from hypoxia-treated cells exhibited greater uniformity, dispersion, and stability than those from the normoxic group, resulting in reduced fluctuation under scattered light over time (P≤0.05). The total protein concentration in the hypoxic group was significantly higher than in the normoxic conditions (5.003 mg/ml vs. 4.109 mg/ml, representing a 1.22-fold increase) (P≤0.01). Exosomes extracted under normoxic and hypoxic conditions demonstrated acceptable biocompatibility with no signs of cytotoxicity, irritation, sensitivity, or microbial contamination.Conclusion: Hypoxic preconditioning enhances the yield and physicochemical stability of AM-MSC-derived exosomes, due to their unique composition and functional properties. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Amniotic membrane, Biocompatibility, Extracellular vesicles, Hypoxia, Mesenchymal stem cells, Exosomes</keyword>
				<start_page>544</start_page>
				<end_page>557</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27395.html</web_url>
			<author_list><author>
				<first_name>Hadiseh</first_name>
				<middle_name></middle_name>
				<last_name>Kholgh</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>kholghhadiseh@gmail.com</email>
				<code>120340</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Eshghabadi</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>f.eshghabadi@ut.ac.ir</email>
				<code>120341</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Life Science Engineering, College of Interdisciplinary Science and Technology, University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hanieh</first_name>
				<middle_name></middle_name>
				<last_name>Jafary</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>jafaryh8287@gmail.com</email>
				<code>120342</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Kavosh</first_name>
				<middle_name></middle_name>
				<last_name>Zandsalimi</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>kavosh.bme@yahoo.com</email>
				<code>120343</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Laser (MLRC), Medical Laser Research Center, Yara Institute, ACECR, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nazanin</first_name>
				<middle_name></middle_name>
				<last_name>Akbari</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>nazaninakbarii000@gmail.com</email>
				<code>120344</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, Shahid Beheshti University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Azadeh</first_name>
				<middle_name></middle_name>
				<last_name>Soltani</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>azadehsoltani21@yahoo.com</email>
				<code>120345</code>
				<coreauthor>No</coreauthor>
				<affiliation>Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Banafsheh</first_name>
				<middle_name></middle_name>
				<last_name>Heidari</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>ban_heidari@yahoo.com</email>
				<code>120346</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Regenerative Medicine in Wound Healing, Medical Laser Research Center, Yara Institute, ACECR, 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>Remote ischemic preconditioning protects heart via modulation of purinergic signaling and AMPK-mediated autophagy in rat model of ischemia reperfusion 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): Remote ischemic preconditioning (RIPC) represents a non-invasive, clinically applicable conditioning technique that mitigates myocardial ischemia-reperfusion injury (MIRI). Among various molecular mediators, the adenosine A1 receptor (AA1R) has emerged as a pivotal regulator of cardioprotective signaling. Currently, our aim is to elucidate the contribution of AA1R and AMPK-mediated autophagy in RIPC-induced cardioprotection.Materials and Methods: Prolonged ischemia of 30 min and sustained reperfusion of 120 min were given to isolated hearts of rats using the Langendorff perfusion system to induce MIRI. RIPC was elicited through four intermittent phases of 5-minute hind-limb ischemia and 5-minute reperfusion using a pressure cuff. The role of AA1R and AMPK was investigated via pharmacological inhibition using DPCPX (selective AA1R antagonist) and BML-275 (AMPK inhibitor), respectively.Results: IRI-induced myocardial damage was manifested by a substantial rise in infarct size, elevated levels of cardiac-specific markers, i.e., LDH-1, CK-MB, C-tPn-I, altered hemodynamic parameters (decreased HR, CFR, LVDP, RPP, +dp/dtmax, and -dp/dtmin), and other biochemical markers (increased TBARS, decreased GSH and catalase, increased TNF-α, TGF-β, Bax, and caspase-3). RIPC significantly attenuated these deleterious alterations, restoring both biochemical and functional parameters. However, the administration of DPCPX and BML-275 markedly abrogated the cardioprotective benefits conferred by RIPC.Conclusion: These findings substantiate that RIPC exerts potent cardioprotective effects via activation of AA1R and AMPK-dependent autophagic signaling. The observed interplay between AA1R and AMPK underscores an integrated adaptive mechanism that preserves myocardial integrity during IRI. This mechanistic insight provides a rationale for exploring AA1R-AMPK axis modulation as a therapeutic avenue for clinical cardioprotection. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Adenosine A1 receptor AMP-activated protein- kinase, Autophagy, Cardioprotection, MIRI, Remote ischemic-preconditioning</keyword>
				<start_page>558</start_page>
				<end_page>569</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27397.html</web_url>
			<author_list><author>
				<first_name>Kuldeep</first_name>
				<middle_name></middle_name>
				<last_name>Kumar</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>kuldeepsharmaa1987@gmail.com</email>
				<code>120350</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, (Punjab)-147002, India|Department of Pharmacology, All India Institute of Medical Sciences (AIIMS), New Delhi-110029-India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Harlokesh</first_name>
				<middle_name>Narayan</middle_name>
				<last_name>Yadav</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>hnyadav@gmail.com</email>
				<code>120351</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacology, All India Institute of Medical Sciences (AIIMS), New Delhi-110029-India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nirmal</first_name>
				<middle_name></middle_name>
				<last_name>Singh</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>nirmal_puru@rediffmail.com</email>
				<code>120352</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, (Punjab)-147002, 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>Trans sodium crocetinate protects against hepatotoxicity induced by bisphenol A in 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): Bisphenol A (BPA) is a monomer used in producing a wide range of materials and products, and it is recognized as an endocrine disruptor. Exposure to BPA can cause toxicity in multiple organs, especially the liver. Trans sodium crocetinate (TSC) is a synthetic salt derived from crocetin extracted from Crocus sativus. TSC exhibits antioxidant, anti-apoptotic, and properties that inhibit autophagy. This study evaluates the effects of TSC on liver toxicity induced by BPA.Materials and Methods: A total of 42 rats were allocated into seven groups, including those exposed to BPA at a dose of 75 mg/kg, BPA and trans sodium crocetinate (TSC) at doses of 10, 20, and 40 mg/kg, and groups receiving olive oil, distilled water, or TSC (40 mg/kg) alone. The total antioxidant capacity (TAC), lipid peroxidation, and glutathione, as well as serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and total bilirubin were assessed using colorimetric methods. Reactive oxygen species (ROS) and liver protein expression were quantified using fluorimetric and western blot techniques.Results: TSC, at the dose of 40 mg/kg, reduced the levels of ROS and lipid peroxidation induced by BPA, while remarkably increasing the glutathione content and total antioxidant capacity (TAC) in liver tissue. Moreover, TSC markedly alleviated the BPA-induced increases in caspase-3 protein levels and in the activities of ALT, AST, ALP, and LDH, as well as in serum bilirubin T. Conclusion: Altogether, TSC can be regarded as a supplement to protect against BPA-induced hepatotoxicity due to its potent antioxidant and anti-apoptotic effects. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Anti-oxidant, Apoptosis, Bisphenol A, Oxidative stress, Trans sodium crocetinate</keyword>
				<start_page>570</start_page>
				<end_page>577</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27396.html</web_url>
			<author_list><author>
				<first_name>Majid</first_name>
				<middle_name></middle_name>
				<last_name>keshavarzi</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>keshavarzim2@mums.ac.ir</email>
				<code>120348</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacodynamics and Toxicology, Faculty of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Bibi Marjan</first_name>
				<middle_name></middle_name>
				<last_name>Razavi</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>razavimr@mums.ac.ir</email>
				<code>120347</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Targeted Drug Delivery Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran|Department of Pharmacodynamics and Toxicology, Faculty of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hossein</first_name>
				<middle_name></middle_name>
				<last_name>Hosseinzadeh</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>hosseinzadehh@mums.ac.ir</email>
				<code>120349</code>
				<coreauthor>No</coreauthor>
				<affiliation>Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran|Department of Pharmacodynamics and Toxicology, Faculty 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>Impact of TGF-β and ERK1/2 inhibition on preimplantation embryo development and quality</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): Preimplantation embryo culture is a critical phase in assisted reproductive technologies. The use of small molecules to modulate signaling pathways has emerged as a strategy to improve embryo viability. SB431542 inhibits the TGF-β pathway, while PD0325901 inhibits the MEK/ERK pathway. This study investigates whether their combined application affects embryonic development and cellular composition during early culture, independent of stem cell derivation.Materials and Methods: To assess the effects of SB431542 and PD0325901 on early embryo development, mouse embryos at 2PN, two-cell, and eight-cell stages were collected in vivo and cultured in LIF-supplemented medium containing both molecules until the blastocyst stage. Embryo quality, apoptosis, and developmental progression were assessed using differential staining, TUNEL assay, and continuous monitoring throughout the culture period.Results: Embryos treated with SB431542 and PD0325901 showed a slightly higher rate of blastocyst formation than controls, though the difference was not statistically significant. Degeneration and apoptosis rates were also comparable between groups. However, treated embryos exhibited a significant reduction in ICM cells at early stages, suggesting compromised inner cell mass development. These findings indicate that dual inhibition may not enhance embryo quality under the tested conditions.Conclusion: SB431542 and PD0325901, when applied during preimplantation embryo culture, do not significantly improve developmental progression or reduce degeneration and apoptosis. The observed decrease in ICM cells suggests limited benefit for embryo culture protocols designed to support early development. Further studies are needed to evaluate their relevance in stem cell derivation contexts.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Mitogen-activated protein kinases/Extracellular signal-regulated kinases, PD0325901, Pre-implantation embryo, SB431542, Transforming growth factor- beta</keyword>
				<start_page>578</start_page>
				<end_page>589</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27437.html</web_url>
			<author_list><author>
				<first_name>Faezah</first_name>
				<middle_name></middle_name>
				<last_name>Mohammadi Ghazani</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>faezeh_mohammadi_65@yahoo.com</email>
				<code>120498</code>
				<coreauthor>No</coreauthor>
				<affiliation>Faculty of Development of Biology, University of Science and Culture, Tehran, Iran|Department of Embryology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Shirvanizadeh</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>shirvanizadehfatemeh@yahoo.com</email>
				<code>120499</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Embryology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seyedeh-Nafiseh</first_name>
				<middle_name></middle_name>
				<last_name>Hassani</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>nafiseh.hassani@royaninstitute.org</email>
				<code>120500</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Azam</first_name>
				<middle_name></middle_name>
				<last_name>Dalman</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>dalman79@yahoo.co.uk</email>
				<code>120501</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Embryology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nahid</first_name>
				<middle_name></middle_name>
				<last_name>Nasiri</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>anahid.1333@yahoo.com</email>
				<code>120502</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Embryology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran|Department of Photo Healing and Regeneration, Medical Laser Research Center, Yara Institute Academic Center for Education, Culture and Research (ACECR), Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Maryam</first_name>
				<middle_name></middle_name>
				<last_name>Zarei</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>maryam.zareei@gmail.com</email>
				<code>120503</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Embryology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Saman</first_name>
				<middle_name></middle_name>
				<last_name>Maroufizadeh</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>saman.maroufizadeh@gmail.com</email>
				<code>120504</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biostatistics and Epidemiology, School of Health, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Poopak</first_name>
				<middle_name></middle_name>
				<last_name>Eftekhari Yazdi</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>eftekhari@royaninstitute.org</email>
				<code>120505</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Embryology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, 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>Dexmedetomidine protects against ischemia and reperfusion-induced kidney injury in rats by inhibiting the expression of TRPM2 and TRPA1 channels</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): Renal ischemia and reperfusion (I/R) injury is a potentially serious issue encountered during various medical and surgical procedures. This condition is clinically significant because of its high incidence and mortality rate. In this study, we aimed to investigate the protective effect of dexmedetomidine (DEX) on oxidative stress-activated TRPM2 and TRPA1 channel expression in rats with a renal I/R model.Materials and Methods: A total of 35 rats were used in the study. The animals were divided into five groups. The control group received no procedure during the experiment. In the sham group, the abdomen was opened under general anesthesia, the right kidney was removed, and the left renal pedicle was exposed; however, a renal clamp was not applied. The dexmedetomidine group received dexmedetomidine, using the same surgical procedure. In the I/R groups, rats were subjected to left renal ischemia for 30 min followed by 45 min of reperfusion. Dexmedetomidine was not administered to the I/R group, while dexmedetomidine was given to the I/R+DEX group at the beginning of reperfusion. TRPM2 and TRPA1 levels were analysed in serum and kidney tissues at the end of the experiment.Results: A significant increase in TRPM2 and TRPA1 expression was observed in all samples from the I/R group compared to the non-I/R groups, while a significant decrease in TRPM2 and TRPA1 expression was seen at the I/R+DEX compared to the I/R.Conclusion: Dexmedetomidine may have renoprotective effects in I/R injury by inhibiting redox-TRP channels.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Dexmedetomidine, Ischemia/Reperfusion, Kidney, TRPA1, TRPM2</keyword>
				<start_page>590</start_page>
				<end_page>597</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27455.html</web_url>
			<author_list><author>
				<first_name>Abdulkadir</first_name>
				<middle_name></middle_name>
				<last_name>Uzunboy</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>akuzunboy@hotmail.com</email>
				<code>120595</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Anesthesiology and Reanimation, Faculty of Medicine, Firat University, Elazig, Turkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Tuncay</first_name>
				<middle_name></middle_name>
				<last_name>Kuloglu</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>tkuloglu@firat.edu.tr</email>
				<code>120596</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Medicine, Firat University, Elazig, Turkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Oguzhan</first_name>
				<middle_name></middle_name>
				<last_name>Demirel</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>demireloguzhan1@gmail.com</email>
				<code>120597</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Anesthesiology and Reanimation, Faculty of Medicine, Ankara University, Ankara, Turkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ahmet</first_name>
				<middle_name></middle_name>
				<last_name>TURK</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>aturk@adiyaman.edu.tr</email>
				<code>120598</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Medicine, Adiyaman University, Adiyaman, Turkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Gulsum</first_name>
				<middle_name></middle_name>
				<last_name>Altuntas</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>galtuntas@firat.edu.tr</email>
				<code>120600</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Anesthesiology and Reanimation, Faculty of Medicine, Firat University, Elazig, Turkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Esef</first_name>
				<middle_name></middle_name>
				<last_name>Bolat</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>esefbolat@hotmail.com</email>
				<code>120599</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Anesthesiology and Reanimation, Faculty of Medicine, Firat University, Elazig, Turkiye</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>Comparison of long non-coding RNA NEAT1 expression, P53, and antioxidant factors between Alzheimer’s patients and healthy individuals</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): Several studies have reported that the lncRNA Nuclear-enriched abundant transcript 1 (NEAT1) is associated with the progression of Alzheimer’s disease (AD). Oxidative stress and apoptosis also play crucial roles in the development of AD. The present study compared the serum levels of NEAT1, superoxide dismutase (SOD), glutathione (GSH), and P53 between individuals with AD and healthy controls. Materials and Methods: Peripheral blood samples were collected from 30 AD patients and 33 healthy controls and then centrifuged to separate serum. Total RNAs were isolated, and real-time polymerase chain reaction (RT-qPCR) was applied to determine NEAT1 gene expression. Also, Enzyme-linked immunoassays (ELISA) were conducted to measure SOD and GSH as anti-oxidant factors, and p53 as an apoptosis marker. Results: NEAT1 expression was significantly higher in AD patients than in controls (P&lt;0.001). In addition, ROC analysis revealed that serum NEAT1 levels distinguished AD patients from healthy controls with 90% sensitivity and 84.85% specificity. Moreover, the anti-oxidant levels of SOD (P&lt;0.0001) and GSH (P&lt;0.05) were significantly decreased in AD patients, while P53 levels were significantly increased (P&lt;0.05). However, no significant association was found between NEAT1 expression and the measured blood factors.Conclusion: The serum levels of NEAT1 effectively distinguished between AD patients and non-AD people, underscoring its potential as a blood-based biomarker for the development of Alzheimer’s disease.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Alzheimer disease RNA, Apoptosis, Long non-coding, NEAT1, Oxidative stress</keyword>
				<start_page>598</start_page>
				<end_page>604</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27441.html</web_url>
			<author_list><author>
				<first_name>Sara</first_name>
				<middle_name></middle_name>
				<last_name>Yarahmadi</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>sara.yarahmadiii75@gmail.com</email>
				<code>120517</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran|Cellular and molecular research center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Leila</first_name>
				<middle_name></middle_name>
				<last_name>Alidoust</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>alidoust57@gmail.com</email>
				<code>120518</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Genetics, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Alia</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>alia.saberi@gmail.com</email>
				<code>120519</code>
				<coreauthor>No</coreauthor>
				<affiliation>Neuroscience Research Center, Trauma Institute, Poursina Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Behrooz</first_name>
				<middle_name></middle_name>
				<last_name>Khakpour-Taleghani</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>khakpour_b@yahoo.com</email>
				<code>120520</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran|Neuroscience Research Center, Trauma Institute, Poursina Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohamad</first_name>
				<middle_name></middle_name>
				<last_name>Rostampour</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>rost_v@yahoo.com</email>
				<code>120521</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran|Cellular and molecular research center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Adele</first_name>
				<middle_name></middle_name>
				<last_name>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>jafari.adele@gmail.com</email>
				<code>120522</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Physiology, School of Medicine, Guilan University of Medical Sciences, Rasht, 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>Norepinephrine promotes the proliferation, migration, and phenotypic transformation of renal artery vascular smooth muscle cells via ROCK1</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 investigated the role of norepinephrine (NE) and ROCK1 in regulating renal artery vascular smooth muscle cells (rVSMCs).Materials and Methods: rVSMCs were treated with NE, and ROCK1 expression was assessed. Cell proliferation, migration, and phenotypic switching were evaluated using EdU incorporation and wound-healing assays. ROCK1 was silenced by siRNA. Mitochondrial membrane potential and morphology were analyzed to determine NE-induced mitochondrial alterations.Results: NE significantly up-regulated ROCK1 expression in rVSMCs. It promoted proliferation, migration, and phenotypic switching, as indicated by increased expression of proliferative and migratory markers, whereas ROCK1 silencing attenuated these effects. NE also reduced mitochondrial membrane potential and induced mitochondrial fission, suggesting an additional mechanism contributing to vascular remodeling.Conclusion: NE promotes rVSMCs proliferation, migration, and phenotypic switching through ROCK1 activation and alters mitochondrial dynamics. These findings identify the NE–ROCK1 axis as a critical mediator of vascular remodeling in hypertensive nephropathy and suggest it may serve as a promising therapeutic target.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Hypertensive nephropathy, Mitochondrial fission, Norepinephrine, Rho-associated kinase, Vascular smooth muscle- cells</keyword>
				<start_page>605</start_page>
				<end_page>612</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27453.html</web_url>
			<author_list><author>
				<first_name>Sixuan</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>chensixuan2022@163.com</email>
				<code>120575</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Cardiology,The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China|Department of Geriatrics,The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Lina</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>13351000102@163.com</email>
				<code>120576</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Geriatrics,The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Lu</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>2023020963@hrbmu.edu.cn</email>
				<code>120577</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Geriatrics,The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hui</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>hli0314@163.com</email>
				<code>120578</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Geriatrics,The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Junyao</first_name>
				<middle_name></middle_name>
				<last_name>Lu</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>18904804803@163.com</email>
				<code>120579</code>
				<coreauthor>No</coreauthor>
				<affiliation>The Key Laboratory of Cardiovascular Disease Acousto-Optic Electromagnetic Diagnosis and Treatment in Heilongjiang Province, The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yaxin</first_name>
				<middle_name></middle_name>
				<last_name>He</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>17838825710@163.com</email>
				<code>120580</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Geriatrics,The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yihong</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>1042803526@qq.com</email>
				<code>120581</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of endocrinology, Heilongjiang Province Hospital, Harbin 150088, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yuanyuan</first_name>
				<middle_name></middle_name>
				<last_name>Guo</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>guoyuanyuan@hrbmu.edu.cn</email>
				<code>120582</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Cardiology,The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China|Department of Geriatrics,The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China|The Key Laboratory of Cardiovascular Disease Acousto-Optic Electromagnetic Diagnosis and Treatment in Heilongjiang Province, The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mingyu</first_name>
				<middle_name></middle_name>
				<last_name>Liu</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>liumingyu0504@126.com</email>
				<code>120583</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Cardiology,The First Affiliated Hospital, Harbin Medical University, Harbin 150088, China|The Key Laboratory of Cardiovascular Disease Acousto-Optic Electromagnetic Diagnosis and Treatment in Heilongjiang Province, The First Affiliated Hospital, Harbin Medical University, Harbin 150088, 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>The effect(s) of berberine from Berberis vulgaris L. (Berberidaceae) on treating type 1 diabetes mellitus in streptozotocin-induced diabetic 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): Berberis vulgaris (B. vulgaris) L. (Berberidaceae), deeply rooted in Iranian traditional medicine, exhibits significant antidiabetic potential attributed to its berberine content. This plant has been historically used for its glucose-lowering, anti-oxidant, and anti-inflammatory properties. This research investigated berberine’s capacity to regenerate pancreatic β-cells in type 1 diabetic rats, specifically examining its dose-dependent effects on metabolic recovery, histopathological restoration, and molecular mechanisms underlying β-cell regeneration. Materials and Methods: Two groups of streptozotocin-induced diabetic rats received daily oral berberine (50 and 100 mg/kg) for 60 days. We measured berberine half-life and gamma aminobutyric acid (GABA) levels using high-performance liquid chromatography (HPLC) with ultraviolet-visible (Uv/Vis) and fluorescence detection (FD). Fasting blood sugar (FBS), lipid profiles, liver enzymes, insulin, and gastrin were assessed. Pancreatic histopathology (islet damage) and pancreatic and duodenal homeobox 1 (Pdx1) expression were analyzed.Results: Berberine exhibited a 60-min half-life, with blood concentration declining to 0.63 and 0.95 µmol/l within 90 min. Treatment significantly elevated GABA levels (3.0 and 3.8 mg/dl vs diabetic group: 0.44 mg/dl) and reduced FBS by 50% (327 and 296 mg/dl vs diabetic group: 616 mg/dl). Gastrin levels increased to 8.70 and 8.93 pg/ml (vs diabetic group: 5.96 pg/ml). Histopathology revealed reduced islet shrinkage and vacuolization. Pdx1 expression was increased in the treated groups compared with diabetic controls. Conclusion: Berberine from B. vulgaris effectively stimulates pancreatic β-cell regeneration, as evidenced by restored histoarchitecture, up-regulated Pdx1, and sustained glycemic control despite rapid clearance. This validates its traditional antidiabetic use and positions berberine as a promising disease-modifying agent.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Berberine, Diabetes mellitus type 1, Streptozocin, Gamma-aminobutyric acid, Gastrins, Islets of Langerhans</keyword>
				<start_page>613</start_page>
				<end_page>622</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27440.html</web_url>
			<author_list><author>
				<first_name>Hossein</first_name>
				<middle_name></middle_name>
				<last_name>Salmanizadeh</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.salmanizadeh@ut.ac.ir</email>
				<code>120515</code>
				<coreauthor>No</coreauthor>
				<affiliation>Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Razieh</first_name>
				<middle_name></middle_name>
				<last_name>Yazdanparast</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>ryazdan@ut.ac.ir</email>
				<code>120514</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Institute of Biochemistry and Biophysics (IBB), University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mustafa</first_name>
				<middle_name></middle_name>
				<last_name>Ghanadian</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>ghanadian@pharm.mui.ac.ir</email>
				<code>120516</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacognosy, Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy and Pharmaceutical Sciences, 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>Mechanistic pathways and in silico modeling of gallic acid–mediated protection against doxorubicin-induced nephrotoxicity in 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): This study aimed to evaluate the protective effects of Gallic acid (GA) against (Doxorubicin) DOX-induced renal injury and to explore potential molecular interactions underlying its effects.Materials and Methods: Fifty male rats were randomly assigned to five groups: Control, DOX, GA50+DOX, GA100+DOX, and GA100. DOX was administered as a single intraperitoneal dose on day 8 (40 mg/kg), while GA was given orally at 50 or 100 mg/kg for 10 consecutive days. Renal tissues were collected on day 11 and analyzed for oxidative stress markers, pro- and anti-inflammatory cytokines, and the apoptotic marker caspase-3 via ELISA. Immunohistochemistry assessed Nrf-2 and HO-1 expression, and histopathology evaluated structural alterations. Molecular docking simulations were performed for DOX/topoisomerase IIα (PDB ID: 4FM9) and GA/TNF-α (PDB ID: 2AZ5).Results: GA significantly ameliorated DOX-induced oxidative stress, inflammatory cytokine imbalance, caspase-3 activation, and histological damage in a dose-dependent manner, while enhancing Nrf-2 and HO-1 expression. Docking analysis confirmed DOX binding to topoisomerase IIα and revealed strong GA–TNF-α binding affinity.Conclusion: GA exerts substantial renoprotective effects against DOX-induced nephrotoxicity by modulating oxidative, inflammatory, and apoptotic pathways. The agreement between in vivo findings and in silico modeling supports GA as a potential complementary agent to reduce chemotherapy-related renal injury.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Apoptosis, Doxorubicin, Gallic acid, Inflammation, Molecular docking, Nephrotoxicity, Oxidative stress</keyword>
				<start_page>623</start_page>
				<end_page>633</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27454.html</web_url>
			<author_list><author>
				<first_name>Samet</first_name>
				<middle_name></middle_name>
				<last_name>Teki̇n</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>samet.tekin@atauni.edu.tr</email>
				<code>120584</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Atatürk University, Faculty of Veterinary Medicine, Department of Physiology, 25000 Erzurum, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Burak</first_name>
				<middle_name></middle_name>
				<last_name>Çinar</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>burakcinar@atauni.edu.tr</email>
				<code>120585</code>
				<coreauthor>No</coreauthor>
				<affiliation>Atatürk University, Faculty of Medicine, Department of Medical Pharmacology, 25000 Erzurum, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yusuf</first_name>
				<middle_name></middle_name>
				<last_name>Dağ</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>yusuf_dag02@hotmail.com</email>
				<code>120586</code>
				<coreauthor>No</coreauthor>
				<affiliation>Atatürk University, Faculty of Veterinary Medicine, Department of Physiology, 25000 Erzurum, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Aslıhan</first_name>
				<middle_name></middle_name>
				<last_name>Atasever</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>aslihan.atasever@erzincan.edu.tr</email>
				<code>120587</code>
				<coreauthor>No</coreauthor>
				<affiliation>Atatürk University, Faculty of Veterinary Medicine, Department of Physiology, 25000 Erzurum, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Merve</first_name>
				<middle_name></middle_name>
				<last_name>Bolat</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>mervebolat@atauni.edu.tr</email>
				<code>120588</code>
				<coreauthor>No</coreauthor>
				<affiliation>Atatürk University, Faculty of Veterinary Medicine, Department of Physiology, 25000 Erzurum, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>İsmail</first_name>
				<middle_name></middle_name>
				<last_name>Bolat</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>ismail.bolat@atauni.edu.tr</email>
				<code>120589</code>
				<coreauthor>No</coreauthor>
				<affiliation>Atatürk University, Faculty of Veterinary Medicine, Department of Pathology, 25000 Erzurum, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Burak Batuhan</first_name>
				<middle_name></middle_name>
				<last_name>Laçi̇n</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>bblacin@atauni.edu.tr</email>
				<code>120590</code>
				<coreauthor>No</coreauthor>
				<affiliation>Atatürk University, Faculty of Veterinary Medicine, Department of Physiology, 25000 Erzurum, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Emin</first_name>
				<middle_name></middle_name>
				<last_name>Şengül</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>emin.sengul@atauni.edu.tr</email>
				<code>120591</code>
				<coreauthor>No</coreauthor>
				<affiliation>Atatürk University, Faculty of Veterinary Medicine, Department of Physiology, 25000 Erzurum, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Serkan</first_name>
				<middle_name></middle_name>
				<last_name>Yıldırım</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>syildirim@atauni.edu.tr</email>
				<code>120592</code>
				<coreauthor>No</coreauthor>
				<affiliation>Atatürk University, Faculty of Veterinary Medicine, Department of Physiology, 25000 Erzurum, Turkey|Kyrgyzstan-Turkey Manas University, Faculty of Veterinary Medicine, Department of Pathology, 720007 Bishkek, Kyrgyzstan</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohamad</first_name>
				<middle_name></middle_name>
				<last_name>Warda</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>mohamad.warda@atauni.edu.tr</email>
				<code>120593</code>
				<coreauthor>No</coreauthor>
				<affiliation>Atatürk University, Faculty of Veterinary Medicine, Department of Physiology, 25000 Erzurum, Turkey|Cairo University, Faculty of Veterinary Medicine, Department of Biochemistry, 3753450 Giza, Egypt</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>Synergistic induction of apoptosis in cancer cells by combined silver nanoparticles and paclitaxel</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): Even with treatment, cervical cancer continues to be rampant among females and has the highest mortality. Carrier system therapies, which combine cancer drugs with nanoparticles, are purported to arrest tumor growth and minimize the side effects of cancer drugs. We envisioned paclitaxel-loaded silver nanoparticles (PTX-AgNPs) as an appropriate carrier for targeting cancer cells. Hence, we studied the effects of paclitaxel (PTX) and silver nanoparticles (AgNPs) as an adjunct therapy in the management of cervical cancer.Materials and Methods: Anti-cancer activity with PTX alone or in combination with AgNPs was assessed by MTT assay and real-time PCR. The mechanism underlying the antiproliferative effects was investigated by measuring the expression of apoptotic markers (Bax, Caspase-3, Bak) and anti-apoptotic markers (Bcl-2, Mcl-1) by RT-PCR. Results: PTX and silver nanoparticles alone induced apoptosis; however, at lower doses, they showed synergism, with an inhibitory concentration of 50% (IC50). Real-time PCR showed that the combination treatment, PTX and AgNPs, significantly increased the mRNA expression of the Bax, Bak, and Caspase-3 genes in the HeLa cell line compared with mono-treatment (P&lt;0.05). Anti-apoptotic Bcl-2 and Mcl-1 mRNA levels were also decreased in all treated groups as compared to control cells. Conclusion: We showed that silver nanoparticles have a synergistic effect with PTX and were able to give favorable results (higher cell death in the combined group) at lower concentrations of PTX.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Apoptosis, Hela Cells, Nanoparticles, Paclitaxel, Silver, Uterine Cervical Neoplasms</keyword>
				<start_page>634</start_page>
				<end_page>640</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27438.html</web_url>
			<author_list><author>
				<first_name>Alireza</first_name>
				<middle_name></middle_name>
				<last_name>Shams</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.shams@abzums.ac.ir</email>
				<code>120506</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Anatomy, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad amin</first_name>
				<middle_name></middle_name>
				<last_name>Shams</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>aminshamsrh@gmail.com</email>
				<code>120507</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Medicine, Iran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Maryam</first_name>
				<middle_name></middle_name>
				<last_name>Amirinejad</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>amiri.mm69@gmail.com</email>
				<code>120508</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Anatomy, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ghazale</first_name>
				<middle_name></middle_name>
				<last_name>Molaverdi</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></email>
				<code>120509</code>
				<coreauthor>No</coreauthor>
				<affiliation>Dietary Supplements and Probiotic Research Center, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article>
			</articleset>
			</journal>