<?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>2025</year>
				<month>11</month>
				<day>1</day>
			</pubdate>
			<pubdate>
				<type>gregorian</type>
				<year>2025</year>
				<month>11</month>
				<day>1</day>
			</pubdate>
			<volume>28</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>Recent advances in the genetic engineering of the Leishmania parasite and anti-cancer properties</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[Leishmaniasis is a tropical disease caused by Leishmania species, affecting millions of people worldwide and contributing to substantial morbidity and mortality. Advances in genetic engineering technologies, particularly CRISPR/Cas9, plasmid shuffling, and DiCre-based systems, have significantly enhanced our understanding of Leishmania biology. These approaches have enabled precise gene editing, functional analysis of essential genes, and the development of genetically attenuated strains with potential applications in vaccine design and drug discovery. Gene editing tools have also allowed the identification of key virulence factors and pathways involved in parasite survival and modulation of the host immune system. These insights have opened new directions for therapeutic strategies against leishmaniasis. Interestingly, recent findings highlight notable similarities between leishmaniasis and cancer, including immune checkpoint involvement, chronic inflammation, and shared molecular targets. Leishmania’s ability to influence host immune responses and epigenetic mechanisms mirrors certain cancer-related processes. Moreover, compounds originally developed for cancer treatment, such as miltefosine and topoisomerase inhibitors, have shown effectiveness against Leishmania, supporting the potential for cross-applications. This review outlines recent developments in Leishmania genetic engineering and explores how these advancements can contribute to both anti-leishmanial and anti-cancer therapies. By emphasizing overlapping biological pathways and therapeutic targets, this work suggests innovative approaches to address two major global health challenges.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Attenuated, Host-pathogen interactions, Immunotherapy, Neoplasms, Protozoan Infections, Reverse genetics, Vaccines</keyword>
				<start_page>1447</start_page>
				<end_page>1455</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26544.html</web_url>
			<author_list><author>
				<first_name>Saeid</first_name>
				<middle_name></middle_name>
				<last_name>Rahim</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>saeidrahim74@gmail.com</email>
				<code>116522</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Parasitology and Mycology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hossein</first_name>
				<middle_name></middle_name>
				<last_name>Yousofi Darani</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>yousofidarani@gmail.com</email>
				<code>116523</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Parasitology and Mycology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hossein</first_name>
				<middle_name></middle_name>
				<last_name>Khanahmad</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>hossein_khanahmad@yahoo.com</email>
				<code>116524</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nadia</first_name>
				<middle_name></middle_name>
				<last_name>Pourmoshir</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>pourmoshir.nadia@gmail.com</email>
				<code>116525</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>Bakhshiyani</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.bakhshiani2016@gmail.com</email>
				<code>116526</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Biotechnology, Faculty of Advanced Technologies, Shahrekord University of Medical Sciences, Shahrekord, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sedigheh</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>sedisaberi@med.mui.ac.ir</email>
				<code>116527</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Parasitology and Mycology, School of Medicine, 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>Syringic acid, a promising natural compound for the prevention and management of metabolic syndrome: A systematic review</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[In recent years, because of the changes in modern lifestyles, the incidence of metabolic syndrome (MetS) has been increasing. MetS is a cluster of conditions, including hypertension, insulin resistance, hyperlipidemia, and obesity, that occur together, increasing the risk of cardiovascular diseases (CVDs), stroke, and type 2 diabetes. Therefore, this review provided comprehensive information on the protective effects of SYR on the main components of MetS using natural phenolic acid compounds such as syringic Acid (SYR). An exhaustive search was conducted using keywords related to SYR and MetS in scientific databases like Scopus, Web of Science, PubMed, and Google Scholar from inception to August 2024. The review included all in vitro, in vivo, and clinical research. Preclinical studies showed that SYR has protective effects against MetS, including diabetes, CVDs, dyslipidemia, and obesity. SYR has shown antidiabetic effects in animal models, lowering blood glucose and improving insulin levels. It also mitigated cardiac injury biomarkers, decreased oxidative stress, and improved lipid profiles. In animal models, SYR could lower body weight and fat mass, lower leptin levels, enhance adiponectin circulation, and improve insulin resistance. Nonetheless, there was insufficient clinical research on SYR’s influences on humans undergoing MetS. Further research, especially randomized controlled trials, is needed to examine its effectiveness, safety, optimal doses, and long-term effects. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Diabetes, Dyslipidemia, Hypertension, metabolic syndrome, Obesity, Syringic acid</keyword>
				<start_page>1456</start_page>
				<end_page>1476</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26319.html</web_url>
			<author_list><author>
				<first_name>Habibeh</first_name>
				<middle_name></middle_name>
				<last_name>Mashayekhi-Sardoo</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>habibehmasha@gmail.com</email>
				<code>115531</code>
				<coreauthor>No</coreauthor>
				<affiliation>Bio Environmental Health Hazards Research Center, Jiroft University of Medical Sciences, Jiroft, Iran|Student Research Committee Jiroft University of Medical Sciences, Jiroft, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Sadeghzadeh</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>fsadeghzadeh7@gmail.com</email>
				<code>115532</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee Jiroft University of Medical Sciences, Jiroft, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Maryam</first_name>
				<middle_name></middle_name>
				<last_name>Rameshrad</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>mrameshrad@gmail.com</email>
				<code>115533</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran|Pharmaceutical Research Center, Pharmaceutical Technology Institute, 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>115534</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran|Pharmaceutical 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>Evaluating the effect of fucoidan-alginate combined dressing on wound healing in rats with full-thickness skin removed</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 aims to investigate the effects of fucoidan-alginate combined dressings on wound healing in rats with full-thickness skin defects and to explore the underlying mechanisms. Materials and Methods: Male SD rats were divided into three groups (n=15): Control, 2% fucoidan, and 5% fucoidan. Full-thickness skin wounds were created on each rat. Fucoidan-alginate dressings were prepared by applying 20 mg/ml and 50 mg/ml fucoidan solutions to alginate dressings (2×2 cm), resulting in 2% and 5% (w/v) fucoidan-alginate combined dressings, respectively. The control group utilized alginate dressings. Wound healing was assessed through various methods, including wound area measurement, histopathological analysis, white blood cell counts, ELISA for TNF-α and IL-1β, Masson’s trichrome staining for collagen, immunohistochemistry for TGF-β1, and western blotting for TGF-β1 and Smad-related proteins.Results: The results revealed that wound healing was significantly more effective in rats treated with 5% fucoidan-alginate combined dressings. Compared to the control group (P&lt;0.01) and the 2% FUC group (P&lt;0.05), the 5% FUC group exhibited reduced inflammatory cell infiltration and lower levels of TNF-α and IL-1β. Moreover, in comparison to the control group, the 5% FUC group demonstrated a significant up-regulation in the mean density of TGF-β1 (P&lt;0.01) and significantly elevated protein expression levels of Col I, α-SMA, and p-Smad2/3 (P&lt;0.01). Additionally, a notable amount of collagen production was observed.Conclusion: The findings suggested that fucoidan-alginate dressings promote wound healing, reduce inflammation, and enhance collagen synthesis in rats, likely via the TGF-β1/Smad signaling pathway.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Alginate, Combined Dressing Fucoidan, Natural product, Wound healing</keyword>
				<start_page>1477</start_page>
				<end_page>1485</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26341.html</web_url>
			<author_list><author>
				<first_name>Guifa</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>wangguifa0323@163.com</email>
				<code>115624</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biochemistry and Molecular Biology, School of Basic Medicine, Qingdao University, 308 Ningxia Road, Qingdao, 266071, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nan</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>zhangnan0784@163.com</email>
				<code>115625</code>
				<coreauthor>No</coreauthor>
				<affiliation>2Department of Nutrition and Food Hygiene, School of Public Health, Qingdao University, 308 Ningxia Road, Qingdao, 266071, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Xiaochen</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>13165007702@163.com</email>
				<code>115626</code>
				<coreauthor>No</coreauthor>
				<affiliation>Adelaide 128 Waymouth St, Y Suites on Waymouth Adelaide SA 5000 Australia</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zihan</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>qdgzh2020@163.com</email>
				<code>115627</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Nutrition, The Second People’s Hospital of Lianyungang, Lianyungang, 222000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Man</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>lium_summer@126.com</email>
				<code>115628</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Nutrition and Food Hygiene, School of Public Health, Qingdao University, 308 Ningxia Road, Qingdao, 266071, China|School of Nursing, Qingdao University, 308 Ningxia Road, Qingdao, 266071, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Meilan</first_name>
				<middle_name></middle_name>
				<last_name>Xue</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>snowml@126.com</email>
				<code>115629</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Biochemistry and Molecular Biology, School of Basic Medicine, Qingdao University, 308 Ningxia Road, Qingdao, 266071, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hui</first_name>
				<middle_name></middle_name>
				<last_name>Liang</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>qdlianghui@126.com</email>
				<code>115630</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Nutrition and Food Hygiene, School of Public Health, Qingdao University, 308 Ningxia Road, Qingdao, 266071, 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>Impact of trehalose and hydroxychloroquine on the function of BRAF (V600E)-siRNA in the A375 melanoma 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): Melanoma, a lethal form of skin cancer, is closely linked to mutations in melanocytes. Due to increased resistance to chemotherapy, innovative strategies, including gene and combination therapies, are being explored. This study evaluates the effects of trehalose (TRE) and hydroxychloroquine (HCQ) in enhancing the efficacy of BRAF (V600E)-siRNA in A375 cells.Materials and Methods: The A375 cells were treated, and changes in cell viability were assessed using MTT assays. Apoptosis was evaluated using flow cytometry. Additionally, gene expression analysis of B-Raf proto-oncogene, serine/threonine kinase (BRAF), Caspase 3 (CASP3), and Phosphoinositide-3-kinase regulatory subunit 3 (PIK3R3) was performed using quantitative RT-PCR.Results: HCQ treatment reduced cell viability and increased apoptosis compared to both control cells and cells treated with TRE. Gene expression analysis showed a significant down-regulation of BRAF expression in cells treated with HCQ and BRAF (V600E)-siRNA compared to siRNA-only treated cells. CASP3 expression was significantly up-regulated in cells treated with combined HCQ and siRNA, indicating a stronger apoptotic response. PIK3R3 expression showed no significant change in the transfected groups.Conclusion: TRE, either alone or combined with siRNA, showed limited efficacy and may counteract the apoptotic benefits of HCQ. Conversely, HCQ, whether used alone or in combination with siRNA, enhanced apoptosis, suggesting promise as a potential treatment for melanoma.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>BRAF (V600E), Hydroxychloroquine, Melanoma, siRNA, Trehalose</keyword>
				<start_page>1486</start_page>
				<end_page>1494</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26667.html</web_url>
			<author_list><author>
				<first_name>Elmira</first_name>
				<middle_name></middle_name>
				<last_name>Toobchi</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>eli.tp995@gmail.com</email>
				<code>117054</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Genetics and Molecular Biology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Rana</first_name>
				<middle_name></middle_name>
				<last_name>Moradian Tehrani</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>moradian@med.mui.ac.ir</email>
				<code>117055</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Genetics and Molecular Sciences, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammadreza</first_name>
				<middle_name></middle_name>
				<last_name>Sharifi</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>mo_sharifi@med.mui.ac.ir</email>
				<code>117056</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Genetics and Molecular biology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Tabandeh</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>fatemehtabandehfv.7593@gmail.com</email>
				<code>117057</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Genetics and Molecular biology, Faculty of Medicine, Isfahan university of Medical Sciences, Isfahan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Negin</first_name>
				<middle_name></middle_name>
				<last_name>Hadisadegh</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>neginhadisadegh1998@gmail.com</email>
				<code>117058</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biophysics, Faculty of Biological Sciences, 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>Linalool vs linalool-loaded chitosan nanoparticles in an Aβ-induced rat model of Alzheimer’s disease: A molecular, biochemical, histological, and behavioral study</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): Recent studies have increasingly focused on applying nanotechnology to treat neurodegenerative diseases. In this study, we compared the effects of the monoterpene linalool and linalool-loaded chitosan nanoparticles on key pathological features of Alzheimer’s disease (AD), including oxidative stress, neuroinflammation, neuronal death, amyloid plaque deposition, alterations in tryptophan metabolism, and memory deficit in a rat model of AD. Materials and Methods: An intracerebroventricular injection of Aβ42 (10 µg) was used to induce the AD model. Linalool (25 mg/kg) and nano-linalool (25 mg/kg) were administered orally once daily for 30 consecutive days. Results: Both linalool and nano-linalool significantly reduced malondialdehyde levels and enhanced superoxide dismutase activity in the hippocampus. They also decreased the mRNA levels of monocyte chemoattractant protein-1, inhibited the up-regulation of beta-secretase, reduced amyloid plaque deposition, and attenuated pyramidal neuron death in the CA1 region. Additionally, treatment with both compounds down-regulated indoleamine 2,3-dioxygenase, lowered kynurenine levels, and increased serotonin concentrations in the hippocampus. Although both treatments improved learning and spatial memory in Aβ-injected rats, nano-linalool’s effectiveness was more significant than that of linalool in modulating the molecular, biochemical, and histological parameters.Conclusion: Encapsulating linalool in chitosan nanoparticles enhances its effectiveness in improving molecular, biochemical, and histological changes in the hippocampus of rat models of AD.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Alzheimer’s disease, Amyloid precursor protein - secretases, Hippocampus, Kynurenine, Linalool-loaded chitosan - nanoparticle, Oxidative stress, Spatial Memory</keyword>
				<start_page>1495</start_page>
				<end_page>1504</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26445.html</web_url>
			<author_list><author>
				<first_name>Mohammad</first_name>
				<middle_name></middle_name>
				<last_name>Pakdel</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>mohamadpakdel108@gmail.com</email>
				<code>116068</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, SR.C., Islamic Azad University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Masoumeh</first_name>
				<middle_name></middle_name>
				<last_name>Asle Rousta</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>mrousta58@gmail.com</email>
				<code>116069</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Physiology, Za.C., Islamic Azad University, Zanjan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mehdi</first_name>
				<middle_name></middle_name>
				<last_name>Sadegh</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.sadegh@arakmu.ac.ir</email>
				<code>116070</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Akram</first_name>
				<middle_name></middle_name>
				<last_name>Eidi</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>akram_eidi@yahoo.com</email>
				<code>116071</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, SR.C., Islamic Azad 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>Effect of TGF-β1 transfected dental pulp derived mesenchymal stem cells on in vivo cartilage regeneration</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 investigate the effect of TGF-β1-transfected dental pulp-derived mesenchymal stem cells (DP-MSCs) on the regeneration of osteochondral defects in rabbit knee joints.Materials and Methods: A total of 32 New Zealand white rabbits (3-4 months old, 2-3 kg) were randomly divided into four groups (n=8 per group). Osteochondral defects were surgically created in the distal femoral articular cartilage of three experimental groups, while the control group remained untreated. Group 2 received an intra-articular injection of 0.5 ml sterile saline. Group 3 was administered 0.5 ml of saline containing 3×106 DP-MSCs. Group 4 received 3×106 TGF-β1-transfected DP-MSCs suspended in 0.5 ml of saline. After six weeks, animals were euthanized, and femoral joints were harvested. Tissue sections (5 μm) were analyzed histologically using hematoxylin-eosin, Masson’s trichrome, and Toluidine blue staining, as well as immunohistochemical methods.Results: Histological analysis revealed increased fibrous cartilage in the DP-MSC group compared to the saline group, with some irregular hyaline cartilage regions and dispersed chondrocytes. The TGF-β1+DP-MSC group demonstrated a more significant improvement, characterized by enhanced hyaline cartilage formation and a more organized tissue architecture.Conclusion: TGF-β1 transfection enhances the chondrogenic potential of mesenchymal stem cells by stimulating reparative cellular mechanisms and promoting the formation of hyaline cartilage, thereby facilitating more effective tissue regeneration. These findings suggest that this strategy holds considerable potential for clinical application in cartilage repair and regeneration.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>cartilage regeneration, Dental pulp, Mesenchymal stem cells, Osteochondral defects, TGF-β1</keyword>
				<start_page>1505</start_page>
				<end_page>1515</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26550.html</web_url>
			<author_list><author>
				<first_name>Betül</first_name>
				<middle_name></middle_name>
				<last_name>Tekin Alpargu</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>betus.t.87@gmail.com</email>
				<code>116549</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Medicine, Erciyes University, Kayseri, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Saim</first_name>
				<middle_name></middle_name>
				<last_name>Ozdamar</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>sozdamar@pau.edu.tr</email>
				<code>116550</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Medicine, Pamukkale University, Denizli, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zeynep Burcin</first_name>
				<middle_name></middle_name>
				<last_name>Gonen</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>zeynepburcin@erciyes.edu.tr</email>
				<code>116551</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Oral and Maxillofacial Surgery, Genome and Stem Cell Center (GENKOK), Erciyes University, Kayseri, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ayca</first_name>
				<middle_name></middle_name>
				<last_name>Kara</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>aycakara@erciyes.edu.tr</email>
				<code>116552</code>
				<coreauthor>No</coreauthor>
				<affiliation>Genome and Stem Cell Center (GENKOK), Erciyes University, Kayseri, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hasan</first_name>
				<middle_name></middle_name>
				<last_name>Salkın</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>hasansalkin@beykent.edu.tr</email>
				<code>116553</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Medicine, Istanbul Beykent University, Istanbul, Türkiye</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>Pretreatment with a ketogenic diet inhibits mitochondrial damage in rat models of spinal cord injury via the PGC-1α/Sirt1/Nrf1 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): Spinal cord injury (SCI) often results in poor recovery prospects and a high disability rate. Although the ketogenic diet (KD) was suggested as a neuroprotective agent after SCI, its underlying mechanism remains unclear. Materials and Methods: Rats were divided into three groups: sham-operated controls, SCI with standard diet (SD), and SCI with KD. Following a 2-week dietary pretreatment, the SD and KD groups underwent a cervical level 5 hemi-contusion injury, and their neuromotor functions were monitored for 28 days. The expression levels of PGC-1α, Sirt1, Nrf1, and TOMM20 in the spinal cord tissues were measured using qPCR and immunofluorescence staining.Results: Compared with the SD group, KD pretreatment significantly improved neuromotor recovery and reduced neuronal apoptosis. The expression levels of PGC-1, Sirt1, and Nrf1 in the spinal cord tissues of rats in the KD group were significantly up-regulated. Additionally, KD was found to alleviate neuronal mitochondrial dysfunction by regulating TOMM20 expression.Conclusion: KD pretreatment enhances SCI recovery by modulating the PGC-1α/Sirt1/Nrf1 pathway, improving mitochondrial function, and reducing neuronal death. The study provides new insights into the mechanisms of KD.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Apoptosis, Ketogenic diet, Mitochondria, Sirtuin 1, Spinal cord injury</keyword>
				<start_page>1516</start_page>
				<end_page>1522</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26416.html</web_url>
			<author_list><author>
				<first_name>Xiaomeng</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>xiaomeng8934@163.com</email>
				<code>115957</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Spinal Surgery, Affiliated Longyan First Hospital of Fujian Medical University, Longyan, 364000, Fujian, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Weibin</first_name>
				<middle_name></middle_name>
				<last_name>Lan</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>jinjun478@163.com</email>
				<code>115958</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Spinal Surgery, Affiliated Longyan First Hospital of Fujian Medical University, Longyan, 364000, Fujian, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yang</first_name>
				<middle_name></middle_name>
				<last_name>Liao</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>liqianmo23@163.com</email>
				<code>115959</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Radiology, Affiliated Longyan First Hospital of Fujian Medical University, Longyan, 364000, Fujian, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Haichuan</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>luhaichuan8934@163.com</email>
				<code>115960</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Spinal Surgery, Affiliated Longyan First Hospital of Fujian Medical University, Longyan, 364000, Fujian, 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>Silymarin exerts antipsoriatic effects against imiquimod-induced psoriasis in mice via NF-kB/TLR4 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): Psoriasis is an autoimmune disease that mainly affects the skin and joints, which is mediated via T-cells. Several factors contribute to its pathogenesis, including genetic and environmental triggers, as well as intrinsic immune processes that lead to an autoimmune response. Silymarin, a flavonoid complex extracted from Silybum marianum, exhibits anti-inflammatory, immunostimulatory, and anti-oxidant properties, rendering it a viable candidate for treating psoriasis.This study aimed to investigate the effect of silymarin on imiquimod (IMQ) induced psoriasis-like skin lesions in male mice applied as a cream for seven consecutive days (1 mg per mouse).Materials and Methods: Thirty-five male mice were assigned to seven groups (n=5 per group): (I) control group, (II) IMQ group, (III-V) oral silymarin groups (30, 60, and 120 mg/kg), (VI) topical betamethasone group, and (VII) topical silymarin 2% group. Results: Silymarin, both orally and topically, significantly reduces erythema, thickness, and scaling induced by IMQ after seven days of treatment. The treatment also reversed the increase in spleen weight/body weight ratio. Immunofluorescence analysis revealed that silymarin reduced the expression of nuclear factor κB (NF-κB) (P&lt;0.01) and toll-like receptor 4 (TLR4) (P&lt;0.01) compared to the IMQ group.Conclusion: These findings suggest that silymarin effectively alleviates psoriasis lesions by reducing inflammation and modulating the TLR4/ NF-κB signaling pathway.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Imiquimod, Inflammation, male mice, Psoriasis, Silymarin</keyword>
				<start_page>1523</start_page>
				<end_page>1530</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26543.html</web_url>
			<author_list><author>
				<first_name>Behnaz</first_name>
				<middle_name></middle_name>
				<last_name>Azimi</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>behnazazimi00@gmail.com</email>
				<code>116517</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>Amir</first_name>
				<middle_name></middle_name>
				<last_name>Kiani</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>amir1kiani@yahoo.com</email>
				<code>116518</code>
				<coreauthor>No</coreauthor>
				<affiliation>Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran|Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Tayebeh</first_name>
				<middle_name></middle_name>
				<last_name>Noori</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>tayebehnoori94@gmail.com</email>
				<code>116519</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>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>116520</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 Mallorca E-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>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>116521</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_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>Troxerutin attenuates LPS-induced inflammation in BV2 microglial cells involving Nrf2 activation and NF-κB pathway inhibition</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): Microglial cell-mediated neuroinflammation is a key driver of central nervous system (CNS) homeostasis and a significant risk factor for neurodegeneration and development of neurological diseases. We assessed whether troxerutin (TX) exerts anti-neuroinflammatory effects in lipopolysaccharide (LPS)-stimulated BV2 microglia and explored its mechanism.Materials and Methods: To investigate the suppressive action of TX on M1 polarization, BV2 cells were stimulated with LPS and then treated with TX or minocycline (MINO). Cell viability was assessed via Cell Counting Kit-8 (CCK-8), and inflammatory cytokines were measured by quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA). Furthermore, the nuclear factor erythroid 2-related factor 2 (Nrf2)/nuclear factor-kappa B (NF-κB) signaling pathway was analyzed by Western blotting (WB) to elucidate the molecular mechanism of the anti-neuroinflammatory activity of TX.  Results: TX inhibited the expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β), as well as the secretion of IL-6 and tumor necrosis factor-α (TNF-α). Additionally, TX accelerated the release of transforming growth factor-β (TGF-β) and cluster of differentiation 206 (CD206) in BV2 microglia exposed to LPS. TX regulated the neuroinflammatory response by blocking phosphorylation of NF-κB and inhibitor of kappa B alpha (IκBα) mediated by LPS stimulation and inducing Nrf2 and heme oxygenase-1 (HO-1) protein expression.Conclusion: TX suppresses pro-inflammatory induction after LPS stimulation of BV2 microglia, which may be related to the NF-κB inhibition and accelerated HO-1/Nrf2 activation. These findings pinpoint the potential therapeutic potential of TX in inflammation-induced neurodegenerative diseases.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Anti-inflammatory agents, Lipopolysaccharides, Microglia, Neuroinflammation, NF-kappa B, NRF2 transcription factor</keyword>
				<start_page>1531</start_page>
				<end_page>1538</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26444.html</web_url>
			<author_list><author>
				<first_name>Shengnan</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>jane6386812@126.com</email>
				<code>116062</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmacy, Tianjin Fourth Central Hospital, Tianjin 300140, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hongguang</first_name>
				<middle_name></middle_name>
				<last_name>Fan</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>fan6hg@163.com</email>
				<code>116063</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurology, Tianjin Fourth Central Hospital, Tianjin 300140, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jianhong</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>zhang_jianhong66@sina.com</email>
				<code>116064</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacy, Tianjin Fourth Central Hospital, Tianjin 300140, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Lijun</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>wlj2004497@163.com</email>
				<code>116065</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurology, Tianjin Fourth Central Hospital, Tianjin 300140, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Haiwen</first_name>
				<middle_name></middle_name>
				<last_name>Shi</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>haiwenshitj@163.com</email>
				<code>116066</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacy, Tianjin Fourth Central Hospital, Tianjin 300140, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Changjun</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>lchj0916@163.com</email>
				<code>116067</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacy, Tianjin Fourth Central Hospital, Tianjin 300140, 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>Anti-inflammatory and immunomodulatory effects of camel milk exosomes (CM-Exo) in rat models for burn 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): Camel milk contains proteins with several beneficial characteristics, such as immune-modulating and anti-oxidant effects. Recent research has shown that these benefits are primarily due to extracellular nanovesicles called exosomes. This study aimed to assess the wound-healing capabilities of camel milk exosomes (CM-Exo). Materials and Methods: CM-Exo was extracted, and its size and morphology were examined using DLS, TEM, and SEM. The anti-oxidant properties were assessed using a spectrophotometric (DPPH, FRAP) assay. The MTT test was used to evaluate the viability of human dermal fibroblasts (HDFs) after exposure to high concentrations (HCM-Exo) and low concentrations (LCM-Exo) of milk-Exo. Additionally, a scratch assay analyzed wound closure rate, and the expression of wound healing-associated genes (IL-6 and VEGF-A) was determined using quantitative real-time PCR. We also assessed the healing effects of a topical HCM-Exo ointment on burn-induced rat wounds over 14 days.Results: DLS, TEM, and SEM analyses showed that CM-Exo had an average size of &gt;100 nm with a characteristic spherical shape. The average anti-oxidant activity, as measured by DPPH and FRAP assays, was higher in the HCM-Exo group compared to the LCM-Exo group. HCM-Exo and LCM-Exo enhanced the viability of HDFs, leading to quicker wound closure in an in vitro model. We found an up-regulation of essential wound healing-related genes (IL-6 and VEGF-A) indicative of an ameliorated healing effect. Evaluation of lesion size and histological data indicated a significant reduction in lesion size in the HCM-Exo and 1% silver sulfadiazine cream (Exo+SS) group compared to both the 1% silver sulfadiazine (SS) group and the negative control (Ctrl) group across days 0, 3, 7, and 14. Conclusion: Our study concluded that HCM-Exo significantly accelerated wound healing and reduced inflammatory reactions.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Anti-Oxidants, Burn, Camel milk, Exosomes, Fibroblasts, Inflammatory, Wound healing</keyword>
				<start_page>1539</start_page>
				<end_page>1547</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26665.html</web_url>
			<author_list><author>
				<first_name>Ehsaneh</first_name>
				<middle_name></middle_name>
				<last_name>Azaryan</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>ehsaneh.azaryan@gmail.com</email>
				<code>117040</code>
				<coreauthor>No</coreauthor>
				<affiliation>Cellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Asghar</first_name>
				<middle_name></middle_name>
				<last_name>Zarban</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>azarban@bums.ac.ir</email>
				<code>117041</code>
				<coreauthor>No</coreauthor>
				<affiliation>Cardiovascular Diseases Research Center, Birjand University of Medical Sciences, Birjand, Iran|Clinical Biochemistry Department, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Effat</first_name>
				<middle_name></middle_name>
				<last_name>Alemzadeh</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>effat.ealemzadeh@gmail.com</email>
				<code>117042</code>
				<coreauthor>No</coreauthor>
				<affiliation>Infectious Diseases Research Center, Birjand University of Medical Sciences, Birjand, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Esmat</first_name>
				<middle_name></middle_name>
				<last_name>Alemzadeh</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>esmat.alemzadeh@gmail.com</email>
				<code>117043</code>
				<coreauthor>No</coreauthor>
				<affiliation>Infectious Diseases Research Center, Birjand University of Medical Sciences, Birjand, Iran|Department of Biotechnology, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahdieh</first_name>
				<middle_name></middle_name>
				<last_name>Rajabi-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>rajabimmh@gmail.com</email>
				<code>117044</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pathology, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Alireza</first_name>
				<middle_name></middle_name>
				<last_name>Zangooie</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>zangooei65@gmail.com</email>
				<code>117045</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee, Birjand University of Medical Sciences, Birjand, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Samira</first_name>
				<middle_name></middle_name>
				<last_name>Karbasi</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>s.karbasi@bums.ac.ir</email>
				<code>117039</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Cardiovascular Diseases Research Center, Birjand University of Medical Sciences, Birjand, 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 wound healing through hydrogel:  Arthrospira platensis and Chlorella vulgaris in carboxymethyl cellulose/ carboxymethyl chitosan/gelatin matrix with decellularized amniotic membrane in male Wistar 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): Wound healing requires effective biomaterials to overcome the limitations of conventional treatments, especially for full-thickness injuries. This study introduces an innovative hydrogel composed of carboxymethyl cellulose (CMC), carboxymethyl chitosan (CMCS), and gelatin (Gel), enhanced with extracts from Arthrospira platensis (AP) and Chlorella vulgaris (CV). The matrix is further integrated with decellularized amniotic membranes to enhance therapeutic effects.Materials and Methods: Hydrogels were formulated, crosslinked using 1-Ethyl-3-(3-Dimethylaminopropyl)carbodiimide (EDAC), and incorporated with 1% of either AP, CV, or both extracts. The scaffold was subjected to in vitro cell viability, red blood cell hemolysis, blood clotting index, and in vivo assays. The physical and chemical properties of the scaffolds were also evaluated using weight loss, swelling ratio, scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectroscopy, and nuclear magnetic Resonance (NMR) spectroscopy. To analyze wound healing under in vivo conditions, 36 male Wistar rats were used, and histopathological analysis was performed using hematoxylin and eosin staining.Results: In vitro studies demonstrated that AP-loaded hydrogels exhibited faster degradation and a higher release profile (85.25%) compared to CV (68.32%), consistent with AP’s anti-oxidant properties. In vivo assessments on Wistar rats demonstrated that CV hydrogels achieved faster wound closure and better collagen synthesis, reaching 88 ± 2.5 % closure at 14 days versus 81 ± 2.64 % for AP (P&lt;0.05). The CMC/CMCS/Gel/AP 1%/CV 1% hydrogels showed synergistic effects, achieving a 92 ± 2.1 % closure rate (P&lt;0.01).Conclusion: The hydrogels demonstrated strong potential for skin repair, exhibiting good biocompatibility and controlled release; further refinement of the extracts and materials is suggested.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Tissue engineering, Wound healing, Skin regeneration, Scaffold, Arthrospira platensis, Chlorella vulgaris</keyword>
				<start_page>1548</start_page>
				<end_page>1562</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26678.html</web_url>
			<author_list><author>
				<first_name>Rasoul</first_name>
				<middle_name></middle_name>
				<last_name>Kheradmandi</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>rasoulkheradmandi@gmail.com</email>
				<code>117111</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad</first_name>
				<middle_name></middle_name>
				<last_name>Kamalabadi Farahani</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>mkfarahani64@yahoo.com</email>
				<code>117112</code>
				<coreauthor>No</coreauthor>
				<affiliation>Regenerative Medicine Research Center, Shahroud University of Medical Sciences, Shahroud, Iran|Department of Tissue Engineering, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Morteza</first_name>
				<middle_name></middle_name>
				<last_name>Alizadeh</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>mor1361@gmail.com</email>
				<code>117113</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Tissue Engineering and Biomaterials, School of Advanced Medical Sciences and Technologies, Hamadan University of Medical Sciences, Hamadan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nariman</first_name>
				<middle_name></middle_name>
				<last_name>Rezaei</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>nariman.rezaei67@gmail.com</email>
				<code>117114</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sepehr</first_name>
				<middle_name></middle_name>
				<last_name>Zamani</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>zscalpel.2014@gmail.com</email>
				<code>117115</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Arian</first_name>
				<middle_name></middle_name>
				<last_name>Ehterami</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>arian.ehterami@irem.uzh.ch</email>
				<code>117116</code>
				<coreauthor>No</coreauthor>
				<affiliation>Institute for Regenerative Medicine (IREM), University of Zurich, Zurich, Switzerland</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Majid</first_name>
				<middle_name></middle_name>
				<last_name>Salehi</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>msalehi.te1392@gmail.com</email>
				<code>117117</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Regenerative Medicine Research Center, Shahroud University of Medical Sciences, Shahroud, Iran|Department of Tissue Engineering, School of Medicine, Shahroud University of Medical Sciences, Shahroud, 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>Dapagliflozin improves diabetic cardiomyopathy by suppressing the STAT3-YY1 signaling axis in cardiac fibroblasts</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): Cardiac fibroblast (CF) proliferation and activation drive cardiac fibrosis and heart failure. Dapagliflozin (DAPA), a sodium-glucose cotransporter 2 (SGLT2) inhibitor, ameliorates diabetic cardiomyopathy (DCM). We investigated whether DAPA exerts anti-fibrotic and cardioprotective effects on DCM by directly suppressing CF proliferation and activation independent of SGLT2 inhibition. Materials and Methods: CFs were isolated from mouse hearts. Mouse cardiac function and fibrosis were investigated using histological analysis, western blotting, and echocardiography. Additionally, genetic loss-of-function studies were conducted in vitro by small interfering RNA silencing and in vivo by lentivirus-mediated gene knockdown. Results: Compared with high-glucose-treated neonatal rat CFs, genetic loss-of-function of signal transducer and activator of transcription 3 (STAT3) or pretreatment with DAPA dramatically inhibited STAT3 phosphorylation and Yin Yang 1 (YY1) nuclear translocation, alleviated CF proliferation and activation, and reduced fibrosis. In diabetic db/db mice, administration of DAPA remarkably ameliorated diabetes-induced STAT3 activation, YY1 nuclear translocation, CF proliferation and activation, and reduced cardiac fibrosis and dysfunction. These in vitro and in vivo effects of DAPA were ameliorated by colivelin TFA, a potent activator of STAT3. Intriguingly, knockdown of SGLT2 did not have an inhibitory effect on CF proliferation and activation in db/db mice. Conclusion: DAPA reduces cardiac fibrosis and DCM. This may, at least in part, be attributable to the repression of the STAT3-YY1 signaling axis-mediated CF proliferation and activation, independent of SGLT2 inhibition. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Dapagliflozin, Diabetic cardiomyopathy, Fibroblast, Signal transducer and - activator of transcription 3 Yin Yang 1</keyword>
				<start_page>1563</start_page>
				<end_page>1574</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26547.html</web_url>
			<author_list><author>
				<first_name>Xing-Yi</first_name>
				<middle_name></middle_name>
				<last_name>Shen</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>xingyis8121@163.com</email>
				<code>116539</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Cardiology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Nanjing Medical University, Suzhou, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Xi</first_name>
				<middle_name>Ya</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>l13092307770@163.com</email>
				<code>116540</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zuo</first_name>
				<middle_name>Ying</middle_name>
				<last_name>Hu</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>zuoying_hu@126.com</email>
				<code>116537</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hao</first_name>
				<middle_name></middle_name>
				<last_name>Xie</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>xie_hao_08@163.com</email>
				<code>116538</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, 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>Exosomes from miR-149-3p-transfected menstrual blood-derived mesenchymal stem cells ameliorate inflammation and migration of endometriosis 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): Endometriosis carries remarkable social, public health, and financial consequences. Based on two theories of retrograde menstruation and stem cells, menstrual blood-derived stem cells (MenSCs) play a significant role in endometriosis since key genes of critical cellular processes are differentially expressed in the MenSCs of endometriosis and non-endometriosis women (E- and NE-MenSCs, respectively). In this study, E-MenSCs were isolated from the menstrual blood of women with various endometriosis subtypes. We tried to find the proper microRNA (miRNA) and assayed the effects of exosome-encapsulated miRNA on modulating the gene expression profile and functional pattern of E-MenSCs.Materials and Methods: After in silico selection of miR-149-3p using publicly accessible algorithm-based databases, E- and NE-MenSCs were cultured as controls, and the other experimental groups were as follows: E-MenSCs transfected with empty and miRNA vectors (E-MenSC+BB and E-MenSC+miR), and E-MenSCs treated with exosomes derived from non-transfected and miRNA-transfected NE-MenSCs (E-MenSC+Exo and E-MenSC+T-Exo). Then, the expression level of selected genes, the level of interleukins (ILs) and oxygen reactive species (ROS), the protein level of β-catenin and Ki-67, and the migratory ability were assessed through real-time PCR, ELISA, western blot, and scratching tests, respectively.Results: Although both E-MenSCs+T-Exo and E-MenSC+miR showed down-regulation of IL-6, -8, and -10, neither had decreased IL-1β, vascular endothelial growth factor, IDO1, and KRAS levels. Furthermore, only the IL-6 protein level was significantly decreased in the E-MenSC+miR group, but the levels of IL-6, IL-8, ROS, β-catenin, and Ki67 were significantly lower in the E-MenSCs+T-Exo group compared to the E-MenSCs.Conclusion: The potential of exosomes as miRNA carriers could be considered in developing novel endometriosis therapies.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Endometriosis, Exosomes, Inflammation, Mesenchymal stem cells, MicroRNA 149, Migration</keyword>
				<start_page>1575</start_page>
				<end_page>1588</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26577.html</web_url>
			<author_list><author>
				<first_name>Hoda</first_name>
				<middle_name></middle_name>
				<last_name>Fazaeli</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>hodafazaely@yahoo.com</email>
				<code>116683</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, Faculty of Sciences and Converging Technologies, Science and Research Branch, Islamic Azad University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nasim</first_name>
				<middle_name></middle_name>
				<last_name>Hayati Roodbari</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>hayati@srbiau.ac.ir</email>
				<code>116684</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Biology, Faculty of Sciences and Converging Technologies, Science and Research Branch, Islamic Azad University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ehsan</first_name>
				<middle_name></middle_name>
				<last_name>Ehsani</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>ee_ehsan@yahoo.com</email>
				<code>116685</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Biology, Faculty of Sciences, Islamic Azad University, Roudehen Branch, Roudehen, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Azar</first_name>
				<middle_name></middle_name>
				<last_name>Sheikholeslami</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>azareslami10@gmail.com</email>
				<code>116686</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Cell Biology and Regenerative Medicine, Academic Center for Education, Culture and Research (ACECR), Qom branch, Qom, 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>Elucidating the effect of deferoxamine, a hypoxia mimetic agent, on angiogenesis restoration in endothelial progenitor cells (EPCs) from diabetic 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): Diabetes increases the risk of heart disease and stroke, primarily through endothelial cell dysfunction and vascular damage. These vascular complications are partly due to defects in endothelial progenitor cells (EPCs). This study explores the efficacy of pharmacological priming of bone marrow EPCs (BMEPCs) with Deferoxamine (DFO), a hypoxia mimetic agent, in restoring dysregulated angiogenic pathways in streptozotocin (STZ)-induced mice with type-1 diabetes (T1D).Materials and Methods: BMEPCs were isolated from both normal and STZ-induced mice with T1D. The effects of an optimal concentration of DFO (80 µM) on the viability, proliferation, and tubulogenesis of EPCs were assessed. Furthermore, the probable beneficial effects of the conditioned medium from EPCs treated in the presence and absence of DFO were examined in mice (T1D) wound healing models.Results: DFO (80 µM) increased cell viability, proliferation, and tubulogenesis. EPCs isolated from diabetic mice showed significant impairments in the expression of HIF-1α, VEGF, and SDF-1 proteins compared to controls. DFO-preconditioning significantly enhanced protein expression of these genes. The conditioned medium from diabetic EPCs treated with DFO had a substantially greater favorable effect on wound healing in diabetic mice, connected with elevated levels of HIF-1α, VEGF, phosphorylated Tie2/Tie2, and Ang1.Conclusion: DFO reactivates proliferation and restores the impaired angiogenic properties of EPCs from diabetic mice by stabilizing HIF-1α and VEGF. Additionally, DFO enhanced the pro-angiogenic activity in the EPC-secretome, leading to improved wound healing. This improvement is attributed to the dual activation of HIF-1α /VEGF and Ang-1/Tie2 pathways, which are crucial for initiating and maturing new blood vessels.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Deferoxamine, Diabetes, Endothelial progenitor cell HIF-α, Tie2, VEGF</keyword>
				<start_page>1589</start_page>
				<end_page>1597</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26664.html</web_url>
			<author_list><author>
				<first_name>Vahid</first_name>
				<middle_name></middle_name>
				<last_name>Siavashi</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>vahid_siavashi@ut.ac.ir</email>
				<code>117035</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacology and Razi Drug Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran|Department of Clinical Pathology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seyed Mahdi</first_name>
				<middle_name></middle_name>
				<last_name>Nassiri</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>117036</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Pathology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahdi</first_name>
				<middle_name></middle_name>
				<last_name>Farhadi Mahalli</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>mfarahani@ut.edu.my</email>
				<code>117038</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>Tunku</first_name>
				<middle_name></middle_name>
				<last_name>Kamarul</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>tkzre@um.edu.my</email>
				<code>117037</code>
				<coreauthor>No</coreauthor>
				<affiliation>Tissue Engineering Group (NOCERAL), Department of Orthopedic Surgery, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ali</first_name>
				<middle_name>Mohammad</middle_name>
				<last_name>Sharifi</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>sharifalim@gmail.com</email>
				<code>117034</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmacology and Razi Drug Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran|Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran|Stem cell and Regenerative Medicine Research Center, Iran University of Medical Sciences, Tehran, Iran|Tissue Engineering Group (NOCERAL), Department of Orthopedic Surgery, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia</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>Evaluation of myocardial classic and alternative pathways of the renin-angiotensin system in cholestasis-induced cardiac injury: A time-course experimental study 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): Cholestasis, characterized by impaired bile flow and elevated bile acid levels, can lead to cardiac dysfunction, termed Cholecardia syndrome. The pathophysiology of cholestasis-induced cardiac injury involves direct and indirect effects of bile acids through various molecular pathways. However, the role of the renin-angiotensin-aldosterone system (RAS), modulated by bile acids, remains unclear.This study aimed to investigate alterations in the expression of classic and alternative RAS components in the myocardium of rats with obstructive cholestasis in a six-week period.Materials and Methods: Forty-two male Wistar rats (8 weeks old, 250 ± 30 g) were randomly assigned to seven groups (n=6 per group): one sham-operated group and six bile duct ligation (BDL) groups, sacrificed at weekly intervals from 1 to 6 weeks post-surgery. Quantitative RT-PCR was used to analyze cardiac RAS component expression. Biochemical and histopathological evaluations were conducted to assess disease progression.Results: In the classic RAS pathway, myocardial angiotensin-converting enzyme (ACE) expression increased after week 4 of BDL, while angiotensin II type 1 receptor (AT1R) and angiotensin II type 2 receptor (AT2R) were significantly down-regulated in this period. In contrast, the alternative RAS pathway components, including ACE2 and the Mas receptor, exhibited a biphasic expression pattern in the myocardium, with down-regulation at week 3 followed by significant up-regulation at weeks 5–6.Conclusion: The findings reveal distinct alterations in RAS pathways during cholestasis-induced cardiac injury. The alternative RAS pathway may play a compensatory role in late-stage cholestasis, highlighting potential therapeutic targets for Cholecardia syndrome and cirrhotic cardiomyopathy.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Angiotensin-converting - enzyme 2, Angiotensin receptors, Cholecardia syndrome, cholestasis, Renin-angiotensin system</keyword>
				<start_page>1598</start_page>
				<end_page>1606</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26666.html</web_url>
			<author_list><author>
				<first_name>Azadeh</first_name>
				<middle_name></middle_name>
				<last_name>Khalili</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>azadeh8058@yahoo.com</email>
				<code>117046</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology-Pharmacology-Medical Physics, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Parham</first_name>
				<middle_name></middle_name>
				<last_name>Samimisedeh</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>parhamsamimimd@gmail.com</email>
				<code>117047</code>
				<coreauthor>No</coreauthor>
				<affiliation>Cardiovascular Research Center, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad</first_name>
				<middle_name></middle_name>
				<last_name>Maleki</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>khaliliaz8058@gmail.com</email>
				<code>117048</code>
				<coreauthor>No</coreauthor>
				<affiliation>Cardiovascular Research Center, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Elmira</first_name>
				<middle_name></middle_name>
				<last_name>Jafari Afshar</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>elmirafshar72@gmail.com</email>
				<code>117049</code>
				<coreauthor>No</coreauthor>
				<affiliation>Cardiovascular Research Center, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad</first_name>
				<middle_name></middle_name>
				<last_name>Jadidian</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>mohammadjadidian@yahoo.com</email>
				<code>117051</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pathology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Roham</first_name>
				<middle_name></middle_name>
				<last_name>Mazloom</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>rohammazloom@abzums.ac.ir</email>
				<code>117050</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology-Pharmacology-Medical Physics, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Gholamreza</first_name>
				<middle_name></middle_name>
				<last_name>Bayat</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>g.bayat@abzums.ac.ir</email>
				<code>117052</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Physiology-Pharmacology-Medical Physics, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hossein</first_name>
				<middle_name></middle_name>
				<last_name>Karim</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.karim@abzums.ac.ir</email>
				<code>117053</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Cardiovascular Research Center, Alborz University of Medical Sciences, Karaj, Iran|Department of Cardiology, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article>
			</articleset>
			</journal>