<?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>0</year>
				<month>0</month>
				<day>1</day>
			</pubdate>
			<pubdate>
				<type>gregorian</type>
				<year>2025</year>
				<month>4</month>
				<day>1</day>
			</pubdate>
			<volume>28</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>In vitro effects of phytochemicals on adipogenesis with a focus on molecular mechanisms: 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[Adipogenesis, the process of proliferation of adipocyte progenitor cells and their differentiation into mature adipocytes, plays a critical role in the development of obesity. In this context, exploring the effects of phytochemicals on adipogenesis is very promising, as nowadays, they are widely used as food, drink, or supplement and can significantly impact general health and obesity control. This systematic review attempts to evaluate new findings regarding the molecular mechanisms of different phytochemicals on adipogenesis in in vitro models. Between 2010 and July 2023, a comprehensive systematic search of PubMed and Scopus databases was conducted. The following keywords were used: (“adipogenic”) AND (“inhibit” OR “suppress” OR “reduce” OR “anti” OR “decrease”) AND (“cell” OR “cell line” OR “adipocyte”) AND (“phytochemical” OR “plant” OR “herb”). In this review, 109 studies were comprehensively analyzed, which provided important insights into the process of adipogenesis. Among the numerous transcription factors studied, PPARγ, C/EBPα, and SREBP1c were found to be the most important regulators actively involved in adipocyte differentiation. These results highlight the critical role of these factors in the control of adipogenesis and suggest that they represent promising targets for therapeutic interventions aimed at reducing the excessive lipid accumulation associated with obesity. This study provides a compelling rationale for further exploring phytochemicals as potential therapeutics for treating obesity. The potential benefits of using natural products to influence adipogenesis are evident, and future studies should focus on translating these findings into clinical applications. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Adipogenesis, In vitro models, Molecular mechanism, Obesity, Phytochemicals, Systematic review</keyword>
				<start_page>401</start_page>
				<end_page>417</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25564.html</web_url>
			<author_list><author>
				<first_name>Niusha</first_name>
				<middle_name></middle_name>
				<last_name>Kazemi</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>niusha.kazemi7@gmail.com</email>
				<code>112182</code>
				<coreauthor>No</coreauthor>
				<affiliation>Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Elham</first_name>
				<middle_name></middle_name>
				<last_name>Ramazani</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>e.ramazani_bio@yahoo.com</email>
				<code>112183</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, Yazd University, Yazd, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>Tayarani-Najaran</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>tayaraninz@mums.ac.ir</email>
				<code>112184</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Targeted Drug Delivery 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>Vortioxetine exhibits anti-glioblastoma activity via the PI3K-Akt 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): Glioblastoma multiforme (GBM) presents a significant challenge in oncology due to its highly aggressive nature and inherent resistance to conventional therapeutic interventions. Vortioxetine, a novel antidepressant, exhibits anticancer abilities and can traverse the blood-brain barrier. In this study, the antitumor effect and mechanism of vortioxetine on GBM cells were investigated.Materials and Methods: Cell proliferation in GBM cells was assessed using the CCK8 and colony formation assays. Flow cytometry, western blot, and wound healing assay were used to study the mechanisms of vortioxetine. mCherry-GFP-LC3B and confocal microscopy were used to evaluate autophagic activity. RNA sequencing uses the capabilities of high-throughput sequencing methods to provide insight into the transcriptome of cells.Results: Vortioxetine significantly inhibited the proliferation of GBM cells by inducing G1/G0 phase cell cycle arrest. Meanwhile, it also reduced the migratory capabilities of GBM cells. Furthermore, it promoted apoptotic cell death in GBM cells. In addition, it promoted autophagy in GBM cells, and autophagy inhibitors markedly enhanced its antiproliferative activities. Vortioxetine could down-regulate the expressions of PI3K and Akt, which were related to the occurrence and development of GBM. Conclusion: Our findings support the potential of vortioxetine as a novel therapeutic agent for GBM treatment. Vortioxetine exhibits anti-GBM activity via the PI3K-Akt signaling pathway. Meanwhile, our findings reveal autophagy inhibitors as an effective sensitizer for vortioxetine, offering new strategies for treating GBM.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Akt, Apoptosis, Autophagy, GBM, PI3K, Proliferation, Vortioxetine</keyword>
				<start_page>418</start_page>
				<end_page>425</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25513.html</web_url>
			<author_list><author>
				<first_name>Huan-Qi</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>871899896@qq.com</email>
				<code>111982</code>
				<coreauthor>No</coreauthor>
				<affiliation>Research Center for Clinical Pharmacy, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China|Department of Clinical Pharmacology, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Affiliated Hangzhou First People’s Hospital, School of Medicine, Westlake University, Hangzhou 310006, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Dao-Ming</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>22219159@zju.edu.cn</email>
				<code>111983</code>
				<coreauthor>No</coreauthor>
				<affiliation>Research Center for Clinical Pharmacy, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China|Department of Clinical Pharmacology, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Affiliated Hangzhou First People’s Hospital, School of Medicine, Westlake University, Hangzhou 310006, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zhi-Zhen</first_name>
				<middle_name></middle_name>
				<last_name>Huang</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>22419160@zju.edu.cn</email>
				<code>111984</code>
				<coreauthor>No</coreauthor>
				<affiliation>Research Center for Clinical Pharmacy, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China|School of Medicine, Hangzhou City University, Hangzhou 310015, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jing</first_name>
				<middle_name></middle_name>
				<last_name>Cheng</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>22219147@zju.edu.cn</email>
				<code>111985</code>
				<coreauthor>No</coreauthor>
				<affiliation>Research Center for Clinical Pharmacy, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China|School of Medicine, Hangzhou City University, Hangzhou 310015, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Chong</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>zhangchong@hzcu.edu.cn</email>
				<code>111986</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Medicine, Hangzhou City University, Hangzhou 310015, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Neng-Ming</first_name>
				<middle_name></middle_name>
				<last_name>Lin</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>lnm1013@163.com</email>
				<code>111987</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Pharmacology, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Affiliated Hangzhou First People’s Hospital, School of Medicine, Westlake University, Hangzhou 310006, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yang-Ling</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>liyangling1215@163.com</email>
				<code>111988</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Clinical Pharmacology, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Affiliated Hangzhou First People’s Hospital, School of Medicine, Westlake University, Hangzhou 310006, 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>Melittin alleviates bleomycin-induced pulmonary fibrosis in vivo through regulating TGF-β1/Smad2/3 and AMPK/SIRT1/PGC-1α signaling pathways</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): The present study investigated the protective effect of melittin (MEL) against bleomycin (BLM)- induced pulmonary fibrosis (PF) in mice and the mechanism underlying this effect.Materials and Methods: A mouse model of PF was established by intratracheal injection of 3.5 mg/kg BLM. Twenty-four hours after the model was established, the mice in the treatment groups were intraperitoneally injected with MEL, and specimens were collected 28 days later. The body weight, survival rate, and pulmonary index (PI) of the mice were determined. Haematoxylin and eosin (HE) staining, Masson’s trichrome staining, immunohistochemical staining, kit assays, and Western blot (WB) analysis were performed.Results: Our study indicated that MEL significantly increased the body weight and survival rate, reduced PI, and improved lung histopathology in mice. In addition, MEL inhibited epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM) deposition. Attenuated mitochondrial damage and reduced oxidative stress (OS) were also observed in MEL-treated mice. We further showed that MEL inhibited the TGF-β1/Smad2/3 pathway and activated the AMPK/SIRT1/PGC-1α pathway.Conclusion: MEL is a promising future therapeutic agent for PF. Its multifaceted and complex mechanism of action inhibits both EMT and ECM production by modulating the TGF-β1/Smad2/3 pathway. It also improves mitochondrial function and reduces OS at least partially through the activation of the AMPK/SIRT1/PGC-1α signaling pathway.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Epithelial-mesenchymal transition, Melittin, Mitochondria, Oxidative stress, Pulmonary Fibrosis</keyword>
				<start_page>426</start_page>
				<end_page>433</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25234.html</web_url>
			<author_list><author>
				<first_name>Jiawang</first_name>
				<middle_name></middle_name>
				<last_name>Yu</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>20201225@wnmc.edu.cn</email>
				<code>110738</code>
				<coreauthor>No</coreauthor>
				<affiliation>The Fifth Clinical Medical College of Anhui Medical University, Hefei, 230032, China|EICU, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>WeiHua</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>lwh683@126.com</email>
				<code>110739</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>The Fifth Clinical Medical College of Anhui Medical University, Hefei, 230032, China|ICU, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, 241000, 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>Bioinformatics analysis identifies dysregulation of MiR-548F-3p and its hub gene in triple-negative breast cancer</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): Triple-negative breast cancer (TNBC), which affects 15–20% of cases, lacks targeted therapies and poses challenges in treatment. MicroRNAs (miRNAs) are potential biomarkers and therapeutic targets in breast cancer. To unravel its unique regulatory role, this study focused on miRNA microarray analysis, particularly miR-548F-3p, in TNBC samples.Materials and Methods: Using the GSE76275 dataset, gene expression profiles were analyzed using the Affymetrix Human Genome U133 Plus 2.0 Array. Differentially expressed genes (DEGs) were identified using robust preprocessing. Weighted gene co-expression network analysis (WGCNA) explored gene modules and identified hub genes co-expressed with miR-548F-3p. Functional enrichment and protein-protein interaction (PPI) network analyses were conducted. Survival analysis was used to assess the prognostic impact of the identified genes.Results: The study found 224 up-regulated DEGs, with miR-548F-3p exhibiting significant down-regulation. MultimiR identified 400 genes that were targeted by miR-548F-3p. WGCNA revealed a blue co-expression module, with 356 genes targeted by miR-548F-3p. A Venn diagram identified common genes, including VANGL2, BRCC3, ANP32E, and ANLN. Functional enrichment highlighted crucial pathways in TNBC pathogenesis, including mitotic spindle organization, spindle assembly checkpoint signaling, cell cycle, and amino acid (serine) metabolism. PPI network analysis identified hub genes, including FOXM1, KIF23, and CDC20. VANGL2, BRCC3, ANP32E, and ANLN were significantly associated with patient outcomes in survival analysis.Conclusion: This analysis highlighted TNBC’s molecular landscape, emphasizing miR-548F-3p’s regulatory role. The identified genes, VANGL2, BRCC3, ANP32E, and ANLN, offer insights into TNBC pathogenesis and potential therapeutic targets, laying the foundation for understanding their clinical implications in the intricate landscape of TNBC.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Computational biology, Gene expression profiling, microRNAs, Survival analysis, Triple negative breast - neoplasms</keyword>
				<start_page>434</start_page>
				<end_page>443</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25445.html</web_url>
			<author_list><author>
				<first_name>Samira</first_name>
				<middle_name></middle_name>
				<last_name>Behroozi</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>behroozisamira@yahoo.com</email>
				<code>111641</code>
				<coreauthor>No</coreauthor>
				<affiliation>National Institute of Genetic Engineering and Biotechnology (NIGEB), Institute of Medical Biotechnology, Department of Medical Genetics, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahdieh</first_name>
				<middle_name></middle_name>
				<last_name>Salimi</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>salimi@nigeb.ac.ir</email>
				<code>111642</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>National Institute of Genetic Engineering and Biotechnology (NIGEB), Institute of Medical Biotechnology, Department of Medical Genetics, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Najaf</first_name>
				<middle_name></middle_name>
				<last_name>Allahyari Fard</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>allahyar@nigeb.ac.ir</email>
				<code>111643</code>
				<coreauthor>No</coreauthor>
				<affiliation>National Institute of Genetic Engineering and Biotechnology (NIGEB), 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>Pre- and post-traumatic boric acid therapy prevents oxidative stress-mediated neuronal apoptosis in spinal cord 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): In our study, the neuroprotective efficacy of pre- and post-traumatic applications of boric acid (BA) in rats with experimentally induced spinal cord injury (SCI) was investigated.Materials and Methods: The experimental animals were divided into four groups: control group (C), SCI group (SCI), BA-treated group before SCI (BA+SCI), and BA-treated group after SCI (SCI+BA). Forty-eight hours after SCI, biochemical levels of malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and cytochrome c (Cytc) and caspase-3 (Casp3) expressions were measured in the spinal cord tissues and were examined histologically.Results: After SCI, oxidative stress markers, such as MDA, TOS, and OSI, and apoptosis markers Cytc and Casp3 showed an increase in levels compared to Group C. The oxidative stress markers that increased after SCI decreased with BA+SCI application, while Cytc level, one of the apoptosis markers that increased after SCI, decreased in both groups with BA application. Cell, myelin, ependymal damage, and hemorrhage levels increased after SCI compared to Group C. These histological markers increased after SCI and decreased after BA+SCI. BA was found to reduce SCI-induced oxidative stress and oxidative stress-induced apoptosis.Conclusion: BA administered before SCI was shown to be more effective in protecting neural damage.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Apoptosis, Boric acid, Neuroprotective, Oxidative stress, Spinal cord injury</keyword>
				<start_page>444</start_page>
				<end_page>450</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25270.html</web_url>
			<author_list><author>
				<first_name>Turan</first_name>
				<middle_name></middle_name>
				<last_name>Kandemir</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>turankandemir26@gmail.com</email>
				<code>110938</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Neurosurgery, Eskisehir Osmangazi University Faculty of Medicine, Eskisehir, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>İbrahim</first_name>
				<middle_name></middle_name>
				<last_name>Söğüt</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>ibrahim.sogut@gmail.com</email>
				<code>110939</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biochemistry, Demiroglu Bilim University, Medical Faculty, Istanbul, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zeki</first_name>
				<middle_name>Serdar</middle_name>
				<last_name>Ataizi</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>sataizi@gmail.com</email>
				<code>110940</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurosurgery, Eskişehir Yunus Emre State</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Betül</first_name>
				<middle_name></middle_name>
				<last_name>Can</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>betul_cn@yahoo.com</email>
				<code>110941</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Biochemistry, Eskisehir Osmangazi University Faculty of Medicine, Eskisehir, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ayşegül</first_name>
				<middle_name></middle_name>
				<last_name>Oğlakçı İlhan</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>ayseguloi@karatekin.edu.tr</email>
				<code>110942</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Laboratory Techniques, Eldivan Health Services Vocational School, Cankırı Karatekin University, Cankırı, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Dilek</first_name>
				<middle_name></middle_name>
				<last_name>Burukoglu Donmez</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>dburukoglu@yahoo.com</email>
				<code>110943</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Histology and Embryology, Eskisehir Osmangazi University Faculty of Medicine, Eskisehir, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Güngör</first_name>
				<middle_name></middle_name>
				<last_name>Kanbak</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>gkanbak@ogu.edu.tr</email>
				<code>110944</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Biochemistry, Eskisehir Osmangazi University Faculty of Medicine, Eskisehir, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Alpha-pinene ameliorates liver fibrosis by suppressing oxidative stress, inflammation, and the TGF-β/Smad3 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): A monoterpene alpha-pinene possesses anti-oxidant, anti-inflammatory, and anti-apoptotic properties. Here, we investigated the effect of alpha-pinene on molecular, biochemical, and histological changes induced by carbon tetrachloride (CCl4) in the liver of male Wistar rats. Materials and Methods: Animals were divided into four groups: Control, Pinene, CCl4, and CCl4.Pinene. Pinene and CCl4.Pinene groups were given alpha-pinene (50 mg/kg/day) through intraperitoneal (IP) injections for six consecutive weeks. CCl4 and CCl4.Pinene groups received IP injections of CCl4 (2 ml/kg twice weekly for six consecutive weeks).Results: The results revealed that alpha-pinene inhibited enhancing liver enzyme AST (P&lt;0.001), ALT (P&lt;0.001), ALP (P&lt;0.01), and GGT (P&lt;0.001) activity in CCl4.Pinene rats. It reduced malondialdehyde (P&lt;0.05) and nitric oxide (P&lt;0.05) levels and increased the catalase enzyme activity (P&lt;0.05) and glutathione levels (P&lt;0.01) in the liver. Likewise, alpha-pinene suppressed proinflammatory and profibrotic gene expression and prevented significant histological damage and collagen deposition in the liver of these animals. Also, alpha-pinene reduced the expression of TLR4 (P&lt;0.01), NF-κB (P&lt;0.05), PI3K (P&lt;0.05), Akt (P&lt;0.05), mTOR (P&lt;0.01), TGF-β1 (P&lt;0.01), and Smad3 (P&lt;0.01) in the liver of rats receiving CCl4. Conclusion: We concluded that alpha-pinene reduced CCl4-induced liver fibrosis by lowering oxidative stress, suppressing liver inflammation, and inhibiting TLR4/NF-κB, TGF-β/Smad3, and PI3K/Akt/mTOR signaling pathways. Consequently, alpha-pinene may have potential therapeutic value in treating liver diseases.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Alpha-pinene, Carbon tetrachloride, Collagen, Glutathione, Inflammation, Toll-like receptor 4</keyword>
				<start_page>451</start_page>
				<end_page>460</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25488.html</web_url>
			<author_list><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Noroozi</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>farzaneh.norouzi17@gmail.com</email>
				<code>111836</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, Zanjan Branch, Islamic Azad University, Zanjan, 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>111837</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Physiology, Zanjan Branch, Islamic Azad University, Zanjan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Rahim</first_name>
				<middle_name></middle_name>
				<last_name>Amini</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>rahimamini84@gmail.com</email>
				<code>111838</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, Zanjan Branch, Islamic Azad University, Zanjan, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zeinab</first_name>
				<middle_name></middle_name>
				<last_name>Sahraeian</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>biosahraeian58@gmail.com</email>
				<code>111839</code>
				<coreauthor>No</coreauthor>
				<affiliation>Nanobiotechnology Research Center, Zanjan Branch, Islamic Azad University, Zanjan, 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>Lycopene ameliorates diabetes-induced pancreatic, hepatic, and renal damage by modulating the JAK/STAT/SOCS signaling pathway 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): Emerging evidence suggests that the JAK/STAT/SOCS signaling pathway is crucial for maintaining homeostasis, and its dysregulation contributes to diabetes development. This study aimed to evaluate the roles of SOCS-1 and SOCS-3 in the pancreas, liver, and kidney and to explore the involvement of the JAK/STAT pathway in the molecular mechanisms underlying their effects on inflammation and apoptosis, as well as organ injury in a diabetes mellitus (DM) model. Additionally, we sought to elucidate the role of the JAK/STAT/SOCS pathway in mediating the effects of lycopene (LYC).Materials and Methods: Forty Sprague-Dawley rats were divided into control, DM, LYC, and LYC+DM groups. Diabetes was induced in the DM groups using streptozotocin. LYC was administered to the LYC and LYC+DM groups for 30 days. After the study, pancreas, liver, and kidney tissues were analyzed using histopathological, immunohistochemical, and PCR methods.Results: Significant vacuolization and degenerative changes were observed in the DM group’s pancreatic islet cells. Kidney and liver tissues showed hyperemia, hemorrhage, and degenerative changes. Immunohistochemical analysis revealed increased expression of Cas-3, TNF-α, IFN-α, and IL-6, while IL-10 was significantly reduced in the DM group. PCR analysis showed elevated levels of TNF-α and Cas-3, with decreased SOCS-1 and SOCS-3 expression in the DM group.Conclusion: This study highlights the therapeutic potential of targeting the JAK/STAT/SOCS pathway with lycopene, demonstrating its promise in mitigating diabetes and related complications.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Apoptosis, Cytokines, Diabetes Mellitus, Inflammation, Lycopene, Signal transduction</keyword>
				<start_page>461</start_page>
				<end_page>468</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25548.html</web_url>
			<author_list><author>
				<first_name>Ozlem</first_name>
				<middle_name></middle_name>
				<last_name>Ozmen</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>ozlemoz@mehmetakif.edu.tr</email>
				<code>112119</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pathology, Faculty of Veterinary Medicine, Burdur Mehmet Akif Ersoy University, Burdur, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Melda</first_name>
				<middle_name></middle_name>
				<last_name>Şahin</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>meldasahin0510@gmail.com</email>
				<code>112120</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pathology, Faculty of Veterinary Medicine, Burdur Mehmet Akif Ersoy University, Burdur, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Senay</first_name>
				<middle_name></middle_name>
				<last_name>Topsakal</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>stopsakal@pau.edu.tr</email>
				<code>112121</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Endocrinology and Metabolism,University, Pamukkale Faculty of Medicine, Denizli, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Şerife</first_name>
				<middle_name></middle_name>
				<last_name>Taşan</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>vethekserifeagirca@gmail.com</email>
				<code>112122</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pathology, Faculty of Veterinary Medicine, Burdur Mehmet Akif Ersoy University, Burdur, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Uğur</first_name>
				<middle_name></middle_name>
				<last_name>Şahi̇n</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>ugursahin@sdu.edu.tr</email>
				<code>112123</code>
				<coreauthor>No</coreauthor>
				<affiliation>Genetic Research Unit, Innovative Technologies Application and Research Center, Süleyman Demirel University, Isparta, 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>Preventing the rejection of skin allografts by immunomodulatory and regenerative effects of exosomes derived from bone marrow mesenchymal stem cells in mice</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Reducing the immune response to inflammation is vital for successful transplantation, yet chronic graft rejection remains a major issue despite immunosuppressive drugs. This study explored the effect of bone marrow mesenchymal stem cell-derived exosomes on the survival of skin allografts in mice.Materials and Methods: C57BL/6 and BALB/c mice underwent skin allograft surgery, followed by intraperitoneal injection of exosomes, which were compared with groups receiving dexamethasone and no treatment group.Results: On day 3, mild signs of graft rejection appeared in both control groups, while none were seen in the exosome-treated group. By day 14, the grafts were completely rejected in the control groups but showed mild rejection in the treatment group. Histopathology revealed severe rejection signs in the control groups, including epithelial necrosis and inflammation, while the treatment group showed signs of angiogenesis and graft acceptance. Additionally, inflammatory cytokine levels (TNF-α, IL-1β, and IL-6) were lower in the treatment group than in the positive control group, particularly on days 3 and 14.Conclusion: The findings suggest that exosomes can prevent graft rejection and may offer a promising therapeutic approach for solid organ transplantation, though further research is needed to standardize exosome methods and evaluate cost-effectiveness.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Exosome, Immunomodulation, Mice, Mesenchymal stem cells, Regeneration, Transplantation</keyword>
				<start_page>469</start_page>
				<end_page>476</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25466.html</web_url>
			<author_list><author>
				<first_name>Parham</first_name>
				<middle_name></middle_name>
				<last_name>Soufizadeh</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>soufizadehparham@ut.ac.ir</email>
				<code>111733</code>
				<coreauthor>No</coreauthor>
				<affiliation>Biomedical Research Institute, University of Tehran, Tehran, Iran|Gene Therapy Research Center, Digestive Diseases Research Institute, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Gholamreza</first_name>
				<middle_name></middle_name>
				<last_name>Nikbakht Brujeni</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>nikbakht@ut.ac.ir</email>
				<code>111734</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Biomedical Research Institute, University of Tehran, Tehran, Iran|Department of Microbiology and Immunology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad Mehdi</first_name>
				<middle_name></middle_name>
				<last_name>Dehghan</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>mdehghan@ut.ac.ir</email>
				<code>111735</code>
				<coreauthor>No</coreauthor>
				<affiliation>Biomedical Research Institute, University of Tehran, Tehran, Iran|Department of Surgery and Radiology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Massoumeh</first_name>
				<middle_name></middle_name>
				<last_name>Jabbari Fakhr</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>mjabbarifakhr@gmail.com</email>
				<code>111736</code>
				<coreauthor>No</coreauthor>
				<affiliation>Biomedical Research Institute, University of Tehran, Tehran, Iran|Department of Tissue Engineering and Applied Cell Sciences, School of Medicine, Qom University of Medical Sciences, Qom, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Pouya</first_name>
				<middle_name></middle_name>
				<last_name>Houshmand</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>p.houshmand95@gmail.com</email>
				<code>111737</code>
				<coreauthor>No</coreauthor>
				<affiliation>Biomedical Research Institute, University of Tehran, Tehran, Iran|Department of Microbiology and Immunology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahyar</first_name>
				<middle_name></middle_name>
				<last_name>Mohebbi</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>mahyarmohebi.mm@gmail.com</email>
				<code>111738</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Surgery and Radiology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hossein</first_name>
				<middle_name></middle_name>
				<last_name>Aminianfar</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>aminianfar@ut.ac.ir</email>
				<code>111739</code>
				<coreauthor>No</coreauthor>
				<affiliation>Biomedical Research Institute, University of Tehran, Tehran, Iran|Department of Pathology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sirous</first_name>
				<middle_name></middle_name>
				<last_name>Sadeghian Chaleshtori</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.sadeghian@ut.ac.ir</email>
				<code>111740</code>
				<coreauthor>No</coreauthor>
				<affiliation>Biomedical Research Institute, University of Tehran, Tehran, Iran|Department of Internal Medicine, Faculty of Veterinary Medicine, University of Tehran, 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>SIRT5 prevents mitochondrial dysfunction and cardiac hypertrophy induced by RIP140</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): To investigate the effect and mechanism of Sirtuin5 (SIRT5) on mitochondrial dysfunction and cardiac hypertrophy induced by receptor-interacting protein 140 (RIP140).Materials and Methods: The neonatal rat cardiomyocytes (NRCMs) and SD rats were treated with Angiotensin II (Ang II) to induce in vitro and in vivo model of cardiac hypertrophy. RIP140 was overexpressed by adenovirus infection, and SIRT5 was overexpressed by plasmid transfection. RIP140 and SIRT5 were knocked down by siRNA interference. The expression of RIP140, SIRT5, and biomarkers of cardiac hypertrophy were measured by qRT-PCR and western blot. The transcription levels of mitochondrial DNA-encoded genes were detected by qRT-PCR. Cell surface area and mitochondrial membrane potential were respectively detected by rhodamine-phalloidin and tetramethylrhodamine ethyl ester (TMRE) fluorescence analysis. Cellular oxygen consumption and ATP production were investigated using assay kits. All data are from at least three independent experiments.Results: The expression of SIRT5 was down-regulated in NRCMs and hearts treated with Ang II. Overexpression of SIRT5 protected cardiomyocytes from AngII-induced hypertrophy, whereas knockdown of SIRT5 resulted in cardiac hypertrophy. Moreover, since SIRT5 was regulated by the transcriptional coactivator, we also found that SIRT5 could be negatively regulated by the transcriptional corepressor RIP140 in cardiomyocytes. Furthermore, SIRT5 significantly attenuated energy metabolic dysregulation and mitochondrial dysfunction and exerted its protective role on myocardial hypertrophy under the regulation of RIP140.Conclusion: SIRT5 exerts a protective role in mitochondrial dysfunction and cardiac hypertrophy induced by RIP140.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Cardiac hypertrophy, Energy metabolism, Mitochondria, RIP140, SIRT5</keyword>
				<start_page>477</start_page>
				<end_page>485</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25268.html</web_url>
			<author_list><author>
				<first_name>Liying</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>1137984433@qq.com</email>
				<code>110929</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacy, Guangzhou Eighth People’s Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yi</first_name>
				<middle_name></middle_name>
				<last_name>Huang</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>909314624@qq.com</email>
				<code>110930</code>
				<coreauthor>No</coreauthor>
				<affiliation>Guangzhou Special Service Recuperation Center of PLA Rocket Force, Guangzhou, Guangdong, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Qiujuan</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>2411288144@qq.com</email>
				<code>110931</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacy, Guangzhou Eighth People’s Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ye</first_name>
				<middle_name></middle_name>
				<last_name>Hong</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>hongyezcc@163.com</email>
				<code>110932</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacy, Guangzhou Eighth People’s Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Honghui</first_name>
				<middle_name></middle_name>
				<last_name>Zhen</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>953156864@qq.com</email>
				<code>110933</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacy, Guangzhou Eighth People’s Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yanfang</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>yfchen312@126.com</email>
				<code>110934</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmacy, Guangzhou Eighth People’s Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 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>Glutamate receptors within the lateral periaqueductal gray (lPAG): Effects on blood pressure and heart rate in basic and hypotensive hemorrhagic 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): The lateral periaqueductal gray (lPAG) is involved in regulating cardiovascular activity. As glutamate is present in this region, the effect of glutamatergic receptors on cardiovascular functions in basic and hypotensive hemorrhagic (Hem) rats was investigated.Materials and Methods: In both basic and hemorrhagic animals, saline, L-glutamate (L-Glu), and ionotropic receptor antagonists (MK-801 and GYK as NMDA and non-NMDA receptor antagonists, respectively) with and without L-Glu microinjected into the lPAG. The heart rate (HR), mean arterial pressure (MAP), and systolic blood pressure (SBP) were captured, and those changes (Δ) were calculated and analyzed.Results: The results showed that in basic conditions, microinjection of MK-801 and GYK alone did not significantly affect cardiovascular parameters, but L-Glu significantly increased all parameters (P&lt;0.001). However, co-injection of GYK and L-Glu significantly attenuated cardiovascular responses induced by L-Glu (P&lt;0.01), whereas MK-801 did not have effects. In Hem hypotensive condition, injection of MK-801 and GYK alone could not significantly change the cardiovascular responses, while L-Glu alone significantly increased these responses (P&lt;0.001). In this condition, Co-injection of L-Glu with GYK attenuates the pressor effect of L-Glu, but MK-801 did not affect it. Conclusion: Findings suggest an excitatory cardiovascular role of the glutamatergic system of lPAG in normotensive conditions mediated by a non-NMDA receptor. However, in hem hypotensive conditions, the endogenous glutamatergic system of lPAG does not affect hem hypotension, while exogenous glutamate via a non-NMDA receptor could improve cardiovascular responses in this condition. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Cardiovascular system, Glutamate, Hemorrhage, Lateral periaqueductal gray, Non-NMDA receptor</keyword>
				<start_page>486</start_page>
				<end_page>492</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25563.html</web_url>
			<author_list><author>
				<first_name>Vida</first_name>
				<middle_name></middle_name>
				<last_name>Alikhani</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>alikhaniv4013@mums.ac.ir</email>
				<code>112179</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, Faculty of Medicine, Gonabad University of Medical Sciences, Gonabad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Reza</first_name>
				<middle_name></middle_name>
				<last_name>Mohebbati</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>mohebbatir@mums.ac.ir</email>
				<code>112180</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, Faculty of Medicine, Gonabad University of Medical Sciences, Gonabad, Iran|Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad Naser</first_name>
				<middle_name></middle_name>
				<last_name>Shafei</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>shafeimn@mums.ac.ir</email>
				<code>112181</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran|Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Effect of ellagic acid on BDNF/PI3K/AKT-mediated signaling pathways in mouse models of depression</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): The aim of this study is to investigate the possible role of the hippocampal BDNF-PI3K-AKT signaling pathway in the antidepressant-like activity of ellagic acid (EA) in mice.Materials and Methods: Male BALB/C mice were divided into 5 groups; vehicle (0.1 ml/day), sertraline (5mg/kg), EA (1 mg/kg), EA+BKM120 (PI3K inhibitor), EA+MK2206 (AKT inhibitor). EA, sertraline and vehicle were injected intraperitoneally for 14 days. Locomotor activity was determined by open field test. The tail suspension test was used to detect the antidepressant-like effect. After behavioral tests, hippocampal tissue was obtained and Western blot analyzes were performed for BDNF and pAKT1. Results: Sertraline and EA provided a reduction in immobility time in the tail suspension test when compared with the control group. BKM120 and MK2206 administration reversed this effect of EA. No statistical difference was found between groups in terms of locomotor activity. EA treatment caused an increase in hippocampal BDNF and pAKT1 levels in mice. While inhibitory agent administrations did not affect the increase of BDNF induced by EA, MK2206 administration reversed the increase in pAKT1 observed with EA.Conclusion: It has shown that EA has an antidepressant-like effect in mice without changing locomotor activity, and this effect may be mediated by the BDNF-PI3K-AKT signaling pathway.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Akt, BDNF, Depression, Ellagic acid, PI3K</keyword>
				<start_page>493</start_page>
				<end_page>497</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25442.html</web_url>
			<author_list><author>
				<first_name>Aslı</first_name>
				<middle_name>Hatice</middle_name>
				<last_name>Bedel</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>aslibedel@sdu.edu.tr</email>
				<code>111632</code>
				<coreauthor>No</coreauthor>
				<affiliation>Süleyman Demirel University Faculty of Pharmacy Department of Pharmacology, Türkiye|Akdeniz University Faculty of Medicine Department of Medicinal Pharmacology, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Coskun</first_name>
				<middle_name></middle_name>
				<last_name>Usta</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>fcusta@akdeniz.edu.tr</email>
				<code>111633</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Akdeniz University Faculty of Medicine Department of Medicinal Pharmacology, 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>In vitro and in vivo evaluation of photo-induced antileishmanial activity of indocyanine green-loaded nanomicelles</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): Due to its low toxicity and high absorbance in the range of 650 to 900 nm, indocyanine green (ICG) has garnered significant attention for its applications in photodynamic therapy (PDT) and photothermal therapy (PTT). However, its tendency to aggregate in aqueous environments limits its efficacy in both in vitro and in vivo applications. Encapsulating ICG in a biocompatible nanomicelle can improve its aqueous stability and photophysical properties. The present study investigated the synergistic effect of ICG-loaded nanomicelles upon irradiation by an 808-nm laser on Leishmania major (L. major) parasites. Materials and Methods: Initially, a nanomicelle comprised ICG was synthesized and characterized. Then, the temperature increase during irradiation and promastigote viability were evaluated in vitro. Subsequently, the prepared samples’ in vitro dark toxicity and phototoxicity were assessed via the MTS assay. Finally, the in vivo antileishmanial efficacy of the ICG-loaded nanomicelles formulation was investigated in BALB/c mice. Results: The absorbance of ICG-loaded nanomicelles at 808 nm was more than 2 times greater than Free-ICG. Also, the prepared formulation exhibited a mean diameter of ~25 nm and a zeta potential of -2.3 ± 1 mV. The combination of ICG-loaded nanomicelles and 808 nm laser with a power density of 2.5 W cm−2 led to a significant reduction in the survival rate of promastigotes and lesion size of infected mice compared to control groups. Conclusion: The PDT/PTT mediated by ICG-loaded nanomicelles can be considered a promising and efficient therapeutic method for L. major, as it is inexpensive, safe, and easy to implement.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Leishmania major, Nanomedicine, Photodynamic Therapy (PDT), Photosensitizer, Photothermal therapy (PTT)</keyword>
				<start_page>498</start_page>
				<end_page>506</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25489.html</web_url>
			<author_list><author>
				<first_name>Shirin</first_name>
				<middle_name></middle_name>
				<last_name>Jalili</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>jalili.shirin@yahoo.com</email>
				<code>111840</code>
				<coreauthor>No</coreauthor>
				<affiliation>Institute of Police Equipment and Technologies, Policing Sciences and Social Studies Research Institute, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jafar</first_name>
				<middle_name></middle_name>
				<last_name>Mosafer</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>mosaferj901@gmail.com</email>
				<code>111841</code>
				<coreauthor>No</coreauthor>
				<affiliation>Research Center of Advanced Technologies in Medicine, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran|Health Sciences Research Center, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seyed Amin</first_name>
				<middle_name></middle_name>
				<last_name>Mousavinezhad</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>mousavinezhad101@gmail.com</email>
				<code>111842</code>
				<coreauthor>No</coreauthor>
				<affiliation>Research Center for Life &amp; Health Sciences &amp; Biotechnology of the Police, Directorate of Health, Rescue &amp; Treatment, Police Headquarters, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ameneh</first_name>
				<middle_name></middle_name>
				<last_name>Sazgarnia</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>sazgarniaa@mums.ac.ir</email>
				<code>111843</code>
				<coreauthor>No</coreauthor>
				<affiliation>Medical Physics Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad Ali</first_name>
				<middle_name></middle_name>
				<last_name>Mohaghegh</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>mohaghegh1982@yahoo.com</email>
				<code>111844</code>
				<coreauthor>No</coreauthor>
				<affiliation>Health Sciences Research Center, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran|Department of Laboratory Sciences, School of Paramedical Sciences, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mehdi</first_name>
				<middle_name></middle_name>
				<last_name>Hoseini</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>hoseini.mehdi98@gmail.com</email>
				<code>111845</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Radiology Technology, School of Paramedical Sciences, Torbat Heydarieh University of Medical Sciences, Torbat Heydarieh, 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>Ameliorative effect of morin on diclofenac-induced testicular toxicity in rats: An investigation into different signal pathways</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): Diclofenac (Diclo) is a therapeutic agent used in the treatment of pain and inflammatory diseases, but it is also toxic to the human body. Morin is a flavonoid found naturally in plants and has many biological and pharmacological activities, including anti-inflammatory, anti-oxidant, and anticancer activities. This study aimed to investigate the efficacy of Morin in Diclo-induced testicular toxicity. Materials and Methods: Morin (50 mg/kg and 100 mg/kg) was administered orally for five days, while Diclo was administered intraperitoneally at 50 mg/kg on days 4 and 5. Biochemical, molecular, and histological methods were used to investigate oxidative stress, inflammation, apoptosis, and endoplasmic reticulum (ER) stress damage indicators in testicular tissue. Results: Morin treatment attenuated Diclo-induced oxidative stress damage by increasing anti-oxidant levels (SOD, CAT, GPx, GSH, Nrf-2, HO-1, and NQO1) and decreasing MDA levels, an indicator of lipid peroxidation. Morin reduced levels of the inflammatory mediators NF-κB protein. Increases in apoptotic Bax and Caspase-3 by Diclo were reduced by Morin, while decreased antiapoptotic Bcl-2 level was increased. Morin reduced Diclo-induced ER stress injury by decreasing ATF-6, PERK, IRE1, GRP-78, and CHOP levels. Also, Diclo decreased COX-2 levels.Conclusion: Overall, Morin may be an effective treatment of choice for testicular tissue damage associated with Diclo toxicity and may reduce the level of damage.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Apoptosis, Diclofenac, Endoplasmic reticulum stress, Inflammation, Morin, Oxidative stress</keyword>
				<start_page>507</start_page>
				<end_page>515</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25503.html</web_url>
			<author_list><author>
				<first_name>Hasan</first_name>
				<middle_name></middle_name>
				<last_name>Şimşek</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>hasansimsek47@hotmail.com</email>
				<code>111909</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Physiology, Faculty of Medicine, Aksaray University, Aksaray, Türki̇ye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nurhan</first_name>
				<middle_name></middle_name>
				<last_name>Akaras</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>nurhanakaras@aksaray.edu.tr</email>
				<code>111910</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Medicine, Aksaray University, Aksaray, Türki̇ye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Cihan</first_name>
				<middle_name></middle_name>
				<last_name>Gur</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>cihan.gur@atauni.edu.tr</email>
				<code>111911</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Laboratory Techniques, Vocational School of Health Services, Atatürk University, Erzurum, Türki̇ye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sefa</first_name>
				<middle_name></middle_name>
				<last_name>Kucukler</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>sefa.kucukler@atauni.edu.tr</email>
				<code>111912</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Veterinary Biochemistry, Faculty of Veterinary, Atatürk University, Erzurum, Türki̇ye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mustafa</first_name>
				<middle_name></middle_name>
				<last_name>Ileriturk</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.ileriturk@atauni.edu.tr</email>
				<code>111913</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Animal Science, Horasan Vocational College, Atatürk University, Erzurum, Türki̇ye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fatih</first_name>
				<middle_name>Mehmet</middle_name>
				<last_name>Kandemir</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>fmkandemir@aksaray.edu.tr</email>
				<code>111914</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Biochemistry, Faculty of Medicine, Aksaray University, Aksaray, Türki̇ye</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 dipeptidyl peptidase-8/9 to combat inflammation-induced osteoclastogenesis in RAW264.7 macrophages and analysis of anti-osteoclastogenesis potential of chrysin</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): Osteoclasts drive bone resorption under inflammation, with cytokines promoting osteoclastogenesis. The role of proline enzymes like dipeptidyl peptidase-8 and 9 (DPP-8/9) in this process remains unclear. This study aimed to explore the DPP-8/9 involvement in inflammation-driven osteoclastogenesis using the RAW264.7 macrophage model.Materials and Methods: Receptor activator of nuclear factor-κB ligand (RANKL) and lipopolysaccharide (LPS) induced osteoclastogenesis, raising interleukin-6 (IL-6), tumor necrosis factor (TNF-α), and IL-23 levels. Using RAW264.7 cells, DPP-8/9 protein and tartrate-resistant acid phosphatase (TRAPc) were assayed. Antibodies for cluster of differentiation (CD86 and CD206) were used to analyze macrophage polarization, while molecular docking was used to assess flavonoid binding to DPP-8/9. Western blot confirmed DPP-8/9 expression in treated macrophages.Results: Administering RANKL and LPS increased IL-6 and TNF-α levels, significantly promoting osteoclastogenesis in RAW264.7 macrophages. This treatment also elevated the levels of the inflammatory macrophage marker IL-23. Osteoclast formation was confirmed by measuring TRAPc levels in the culture. Analysis of the cell supernatant revealed elevated DPP-8/9 levels in the RANKL+LPS group. Inhibition of DPP-8/9 with 1G244 decreased inflammatory cytokines and TRAPc levels in the cell culture. Molecular docking analysis of various flavonoids identified chrysin as a potential molecule with sufficient binding energy against DPP-8/9, a finding confirmed by blotting assay.Conclusion: This study emphasizes the involvement of DPP-8/9 in inflammatory osteoclastogenesis in RAW264.7 macrophages. Inhibition of DPP-8/9 reduced osteoclastogenesis markers and inflammatory cytokines levels, indicating decreased osteoclast formation. Additionally, chrysin demonstrated potential as an anti-DPP-8/9 agent, highlighting its possible role in future therapeutic strategies targeting inflammation-induced osteoclastogenesis. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Chrysin, Dipeptidyl peptidase 8, Dipeptidyl peptidase 9, Inflammatory - osteoclastogenesis, M1 macrophage, RAW264.7 cells</keyword>
				<start_page>516</start_page>
				<end_page>526</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25487.html</web_url>
			<author_list><author>
				<first_name>Syed Sufian</first_name>
				<middle_name></middle_name>
				<last_name>Ahmad</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>sufsahmad22@gmail.com</email>
				<code>111832</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, Hamdard, New Delhi – 110062, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Faraha</first_name>
				<middle_name></middle_name>
				<last_name>Ahmed</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>ahmedfaraha@gmail.com</email>
				<code>111833</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, Hamdard, New Delhi – 110062, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sayeed</first_name>
				<middle_name></middle_name>
				<last_name>Ahmad</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>sahmad_jh@yaho.co.in</email>
				<code>111834</code>
				<coreauthor>No</coreauthor>
				<affiliation>Bioactive Natural Product Laboratory, School of Pharmaceutical Education and Research, Jamia Hamdard, Hamdard, New Delhi – 110062, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Anuja</first_name>
				<middle_name></middle_name>
				<last_name>Krishnan</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>anujabala@hotmail.com</email>
				<code>111835</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Molecular Medicine, School of Interdisciplinary Science and Technology, Jamia Hamdard, Hamdard, New Delhi – 110062,  India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad Ahmed</first_name>
				<middle_name></middle_name>
				<last_name>Khan</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>khan.ahmed1511@gmail.com</email>
				<code>111831</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, Hamdard, New Delhi – 110062, 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>Role of ENaC in gender-associated differences in blood pressure</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): Sexual dimorphism in blood pressure regulation has been extensively noted in humans, but the underlying mechanisms remain to be fully understood. Our research aims to investigate the possible correlation between gender-associated differences in blood pressure and renal sodium transport. Materials and Methods: We measured male and female mice’s blood pressure, urine, and plasma sodium concentration when fed a regular or high-Na+ diet. After that, their renal sodium transporters were assessed by western blot and immunofluorescence. For further investigation, male mice were castrated to observe the differences in blood pressure and renal sodium transporters compared to normal mice. Results: Male mice exhibited higher blood pressure and lower renal sodium excretion than female littermates. Furthermore, the blood pressure of male mice exhibited a more significant and rapid increase relative to female mice when the diet was switched from control sodium to high sodium. Western blot and immunofluorescent staining revealed that in male mice, the sodium transporters epithelial sodium channel (ENaC) and the upstream kinases SPAK (Ste20-related proline/alanine-rich kinase), OSR1 (oxidative stress response kinase 1), and WNK4 (Lysine-Deficient Protein Kinase 4) were elevated. Beyond that, male mice exhibited lowered blood pressure and reduced abundance of ENaC (α, β, and γ) after castration.Conclusion: ENaC plays a significant role in gender-associated differences in blood pressure and renal sodium reabsorption.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Castration, Epithelial sodium channel, Hypertension, Lysine-deficient protein - kinase, Sex differences</keyword>
				<start_page>527</start_page>
				<end_page>532</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25443.html</web_url>
			<author_list><author>
				<first_name>Guo-feng</first_name>
				<middle_name></middle_name>
				<last_name>Yu</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>6517096@zju.edu.cn</email>
				<code>111635</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Laboratory, Children’s Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China, 310052</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Li-qin</first_name>
				<middle_name></middle_name>
				<last_name>Yu</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>994304702@qq.com</email>
				<code>111636</code>
				<coreauthor>No</coreauthor>
				<affiliation>Qiaosi Branch, First People’s Hospital of Linping District, Hangzhou, Zhejiang Province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Qin-rui</first_name>
				<middle_name></middle_name>
				<last_name>Lai</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>22318126@zju.edu.cn</email>
				<code>111637</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Laboratory, Children’s Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China, 310052</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Wei</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>chweige@zju.edu.cn</email>
				<code>111634</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Clinical Laboratory, Children’s Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China, 310052</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>Corrigendum: MicroRNA miR-188-5p enhances SUMO2/3 conjugation by targeting SENP3 and alleviates focal cerebral ischemia/reperfusion injury in rats</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Corrigendum</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword></keyword>
				<start_page>0</start_page>
				<end_page>0</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_25608.html</web_url>
			<author_list></author_list>
				</article>
			</articleset>
			</journal>