<?xml version="1.0" encoding="utf-8"?>
			<journal>
			<title>Iranian Journal of Basic Medical Sciences</title>
			<title_fa></title_fa>
			<short_title></short_title>
			<subject>Medical Sciences</subject>
			<web_url>https://ijbms.mums.ac.ir/</web_url>
			<journal_hbi_system_id>0</journal_hbi_system_id>
			<journal_hbi_system_user></journal_hbi_system_user>
			<journal_id_issn>2008-3866</journal_id_issn>
			<journal_id_issn_online>2008-3874</journal_id_issn_online>
			<journal_id_pii></journal_id_pii>
			<journal_id_doi></journal_id_doi>
			<journal_id_iranmedex></journal_id_iranmedex>
			<journal_id_magiran></journal_id_magiran>
			<journal_id_sid></journal_id_sid>
			<journal_id_nlai></journal_id_nlai>
			<journal_id_science></journal_id_science>
			<language>en</language>
			<pubdate>
				<type>jalali</type>
				<year>2026</year>
				<month>1</month>
				<day>1</day>
			</pubdate>
			<pubdate>
				<type>gregorian</type>
				<year>2026</year>
				<month>1</month>
				<day>1</day>
			</pubdate>
			<volume>29</volume>
			<number>1</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>Artificial intelligence (AI) in academic publishing: Legitimate use, plagiarism detection, and ethical challenges</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type></content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword></keyword>
				<start_page>1</start_page>
				<end_page>2</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27130.html</web_url>
			<author_list><author>
				<first_name>Leila</first_name>
				<middle_name></middle_name>
				<last_name>Arabi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>arabil@mums.ac.ir</email>
				<code>119140</code>
				<coreauthor>No</coreauthor>
				<affiliation>Nanotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ali</first_name>
				<middle_name></middle_name>
				<last_name>Roohbakhsh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>roohbakhsha@mums.ac.ir</email>
				<code>119141</code>
				<coreauthor>No</coreauthor>
				<affiliation>Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Bizhan</first_name>
				<middle_name></middle_name>
				<last_name>Malaekeh-Nikouei</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>malaekehb@mums.ac.ir</email>
				<code>119142</code>
				<coreauthor>No</coreauthor>
				<affiliation>Nanotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Bibi Sedigheh</first_name>
				<middle_name></middle_name>
				<last_name>Fazly Bazzaz</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>fazlis@mums.ac.ir</email>
				<code>119143</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Ashwagandha (Withania somnifera) in insulin resistance and metabolic syndrome: A literature review on mechanisms</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[Metabolic syndrome is characterized by obesity, insulin resistance, dyslipidemia, and hypertension. Withania somnifera, commonly known as ashwagandha or Indian winter cherry, belongs to the Solanaceae family. W. somnifera, particularly its powdered root, is a fundamental component of traditional Indian medicine. W. somnifera (Ashwagandha) exhibits pharmacological activities, including immunomodulatory, anti-stress, and neuroprotective effects in animal models. Also, preclinical and clinical studies demonstrate its anti-inflammatory and antiviral properties. In rodent studies, ashwagandha regulates apoptosis and modulates reactive oxygen species (ROS) levels as well as mitochondrial activity. Additionally, it improves endothelial function in rats, dogs, and human brain endothelial cells. Research conducted in both living organisms and controlled laboratory conditions has demonstrated that W. somnifera alleviates the symptoms of metabolic syndrome. It positively affects diabetes by inhibiting dipeptidyl peptidase-4 (DPP-4), α-glucosidase, and α-amylase, while simultaneously increasing pancreatic insulin secretion and improving insulin sensitivity in organs. It has a vasodilatory and diuretic effect. Ashwagandha reduces the activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. It modulates the gene expression of peroxisome proliferator-activated receptor (PPAR)-γ. It regulates the gene expression of sterol regulatory element-binding protein (SREBP)-1c and CYP7A1. It increases the secretion of bile acids that eliminate excess cholesterol. It reduces oxidative stress and inflammation while protecting the body from the harmful effects of elevated cholesterol. This study aims to compile a variety of research findings on the effectiveness of ashwagandha in managing metabolic syndrome.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Atherosclerosis, Dyslipidemia, Hypertension, Indian ginseng, metabolic syndrome, Withania somnifera</keyword>
				<start_page>3</start_page>
				<end_page>21</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26668.html</web_url>
			<author_list><author>
				<first_name>Emad</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>emadazimi2001@gmail.com</email>
				<code>117061</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee, Mashhad University of Medical Sciences, Mashhad, 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>117062</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahboobeh</first_name>
				<middle_name></middle_name>
				<last_name>Ghasemzadeh Rahbardar</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ghasemzadeh-mahboobeh@yahoo.com</email>
				<code>117063</code>
				<coreauthor>No</coreauthor>
				<affiliation>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>117064</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>Raspberry protective role in inflammatory diseases: An overview</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[Inflammation is a natural immune response triggered by multiple factors such as pathogens, damaged cells, and toxic substances. These triggers can lead to both acute and chronic inflammatory reactions in different tissues, contributing to the development of several inflammatory disorders, including cardiovascular diseases, neuroinflammation, arthritis, and cancer. Both infectious and non-infectious stimuli activate immune cells and initiate critical inflammatory signaling pathways.Raspberries (Rubus idaeus) are abundant in bioactive constituents, especially polyphenols like anthocyanins, flavanols, phenolic acids, urolithin A, and ellagic acid, all of which possess notable anti-inflammatory and anti-oxidant activities. These compounds have been shown to regulate various inflammatory signaling pathways, including MAPKs, NF-κB, PI3K/Akt, AP-1, IL-6, TNF-α, IL-1β, CD40, nitric oxide (NO), caspases, and the JAK-STAT pathway. Studies have emphasized their broad pharmacological effects, such as anti-inflammatory, anti-oxidant, hepatoprotective, cardioprotective, gastroprotective, anti-obesity, skin depigmenting, and bone-regenerative properties. This review emphasizes mechanistic insights into raspberries’ protective roles in managing inflammatory-related disorders, particularly cardiovascular diseases, neurodegenerative conditions, and cancer, and highlights their therapeutic potential.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Alzheimer’s, Atherosclerosis, Cancer, Cardiovascular, Inflammation, Neuroinflammation, Parkinson’s, Raspberry</keyword>
				<start_page>22</start_page>
				<end_page>33</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26996.html</web_url>
			<author_list><author>
				<first_name>Priyanka</first_name>
				<middle_name></middle_name>
				<last_name>Arya</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sarojarya24@gmail.com</email>
				<code>118505</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Galgotias College of Pharmacy, Greater Noida, U.P., India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Vikram</first_name>
				<middle_name></middle_name>
				<last_name>Sharma</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>director.gcp@galgotiacollege.edu</email>
				<code>118506</code>
				<coreauthor>No</coreauthor>
				<affiliation>Galgotias College of Pharmacy, Greater Noida, U.P., India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Priyanka</first_name>
				<middle_name></middle_name>
				<last_name>Singh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>spriyaa35@gmail.com</email>
				<code>118507</code>
				<coreauthor>No</coreauthor>
				<affiliation>Banasthali Vidyapith, Department of Pharmacy, Rajasthan, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Rahul</first_name>
				<middle_name></middle_name>
				<last_name>Sagar</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>aryarahul844@gmail.com</email>
				<code>118508</code>
				<coreauthor>No</coreauthor>
				<affiliation>AnovIP, New Delhi,110049, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Surabhi</first_name>
				<middle_name></middle_name>
				<last_name>Thapliyal</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>surbhithapliyal07@gmail.com</email>
				<code>118509</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacology, All India Institute of Medical Sciences, Rishikesh 249203, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Manu</first_name>
				<middle_name></middle_name>
				<last_name>Sharma</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>smanu@banasthali.in</email>
				<code>118510</code>
				<coreauthor>No</coreauthor>
				<affiliation>Banasthali Vidyapith, Department of Pharmacy, Rajasthan, 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>Electroacupuncture improves hypoxic stress and energy metabolism to alleviate vascular cognitive impairment through activation of the HIF-1α/p53/NGB 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): We aimed to demonstrate that electroacupuncture (EA) alleviates vascular cognitive impairment (VCI) induced by cerebral ischemia in rats by modulating oxygen homeostasis and energy metabolism through the HIF-1α/p53/NGB signaling pathway.Materials and Methods: Male Sprague‒Dawley rats underwent bilateral common carotid artery occlusion (BCCAO) to establish a VCI model. EA was administered once daily for 30 min over two weeks. Thirty minutes prior to EA, the hypoxia-inducible factor-1α (HIF-1α) inhibitor 2-methoxyestradiol (2ME2) was injected intraperitoneally. Cognitive function following BCCAO and EA was assessed using the Morris water maze test. Western blotting was performed to analyze the protein expression of HIF-1α, heme oxygenase-1 (HO-1), and neuroglobin (NGB). In addition, p53 mRNA expression was quantified by real-time PCR, and energy metabolite levels were determined using ELISA.Results: EA significantly improved learning and memory in VCI model rats. Histopathological analysis revealed that EA attenuated neuronal apoptosis and ultrastructural damage in the cortex and hippocampus. EA upregulated HIF-1α, NGB, and HO-1 expression but downregulated p53 mRNA expression in these regions. Moreover, EA treatment reversed the expression of glucose, lactic acid, and acetone aldehyde. Notably, the beneficial effects of EA on cerebral energy metabolism were abolished by 2ME2 in VCI model rats.Conclusion: EA alleviated BCCAO-induced neurological impairment and cognitive dysfunction in rats, possibly by reducing hypoxic stress and enhancing energy metabolism in the cortex and hippocampus, potentially through modulation of the HIF-1α/p53/NGB signaling pathway.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Electroacupuncture, Energy metabolism, HIF-1α, Hypoxic stress, Vascular cognitive - impairment</keyword>
				<start_page>34</start_page>
				<end_page>42</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26948.html</web_url>
			<author_list><author>
				<first_name>Peijia</first_name>
				<middle_name></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>zjyyhpj@163.com</email>
				<code>118301</code>
				<coreauthor>No</coreauthor>
				<affiliation>The Second Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fangyuan</first_name>
				<middle_name></middle_name>
				<last_name>Xu</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>xfy979606@163.com</email>
				<code>118302</code>
				<coreauthor>No</coreauthor>
				<affiliation>The First Clinical Medical School, Anhui University of Chinese Medicine, Hefei, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Wendong</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>zjzwd1234@sina.com</email>
				<code>118307</code>
				<coreauthor>No</coreauthor>
				<affiliation>The Second Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Lin</first_name>
				<middle_name></middle_name>
				<last_name>Bai</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>515822508@qq.com</email>
				<code>118303</code>
				<coreauthor>No</coreauthor>
				<affiliation>The Second Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fan</first_name>
				<middle_name></middle_name>
				<last_name>Dai</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>daifan13342553558@163.com</email>
				<code>118304</code>
				<coreauthor>No</coreauthor>
				<affiliation>The First Clinical Medical School, Anhui University of Chinese Medicine, Hefei, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yu</first_name>
				<middle_name></middle_name>
				<last_name>Ye</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>yeyu3106604360@163.com</email>
				<code>118305</code>
				<coreauthor>No</coreauthor>
				<affiliation>The Second Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jingji</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>wjjglacial@163.com</email>
				<code>118306</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>The Second Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hongliang</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>chl.75811@163.com</email>
				<code>118308</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>The Second Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, 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>Neuroprotective effects of kojic acid and nano-kojic acid in experimental brain ischemia induced by bilateral common carotid artery occlusion</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): Brain ischemia remains a leading cause of death and neurological disability worldwide, with current treatments limited by narrow therapeutic windows and insufficient neuroprotection. Kojic acid (KA), a natural compound with demonstrated anti-oxidant and anti-inflammatory properties, has not been thoroughly evaluated in cerebral ischemia. Its limited brain bioavailability may have hindered the identification of its potential therapeutic effects. This study aimed to investigate the effects of both KA and its nanostructured lipid carriers (nKA) in a rat bilateral common carotid artery occlusion (BCCAO) model.Materials and Methods: Adult male rats were randomly allocated to seven groups: sham, BCCAO, KA (1 and 10 mg/kg), nKA (1 and 10 mg/kg), and vehicle. Following BCCAO surgery, animals received intraperitoneal treatments for seven days. Behavioral assessments included the modified neurological severity score and grid walk test. Brain and serum samples were collected to evaluate histopathology, gene expression, oxidative stress markers, inflammatory cytokines, and pharmacokinetic parameters.Results: Histological analysis indicated reduced neuronal loss in both KA and nKA-treated groups. Notably, only nKA significantly improved behavioral outcomes. Both treatments reduced the pro-apoptotic gene BAX and the pro-inflammatory cytokine TNF-α, while nKA additionally increased Nrf2 and reduced IL-6 expression. Both formulations mitigated oxidative stress by decreasing reactive oxygen species, protein carbonylation, and malondialdehyde levels, while also increasing glutathione concentrations.Conclusion: Nano-kojic acid showed better neurobehavioral improvements, while both forms reduced oxidative stress and inflammation, indicating neuroprotective potential. Further studies are needed to clarify mechanisms and long-term safety.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Anti-Oxidants, Inflammation, Ischemia, Neuroprotection, Oxidative stress</keyword>
				<start_page>43</start_page>
				<end_page>54</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26950.html</web_url>
			<author_list><author>
				<first_name>Mohammad</first_name>
				<middle_name></middle_name>
				<last_name>Shokati Sayyad</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mohammad.shokati69@gmail.com</email>
				<code>118313</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Majid</first_name>
				<middle_name></middle_name>
				<last_name>Saeedi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>majsaeedi@gmail.com</email>
				<code>118314</code>
				<coreauthor>No</coreauthor>
				<affiliation>Pharmaceutical Sciences Research Center, Institute of Herbal Medicines and Metabolic Disorders, Mazandaran University of Medical Sciences, Sari, Iran|Department of Pharmaceutics, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Shaki</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>fshaki.tox@gmail.com</email>
				<code>118315</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran|Pharmaceutical Sciences Research Center, Institute of Herbal Medicines and Metabolic Disorders, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fereshteh</first_name>
				<middle_name></middle_name>
				<last_name>Talebpour Amiri</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ftaleb2001@yahoo.co.uk</email>
				<code>118316</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Anatomy, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Reza</first_name>
				<middle_name></middle_name>
				<last_name>Negarandeh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>negarandeh.reza@yahoo.com</email>
				<code>118317</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmaceutics, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran|Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad</first_name>
				<middle_name></middle_name>
				<last_name>Seyedabadi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>seyedabadi1981@gmail.com</email>
				<code>118318</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran|Pharmaceutical Sciences Research Center, Institute of Herbal Medicines and Metabolic Disorders, Mazandaran University of Medical Sciences, Sari, 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>Enhancing clomipramine antidepressive effect using nanocomplexes via different routes of administration: A comparative 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): Enhancing clomipramine anti-depressive effect using a nanoformulation and investigating its effect via different routes of administration (oral and intranasal) in a depression rat model. Polyelectrolytes nanocomplexes (NC) were prepared by an all-aqueous technique and were composed of different ratios of chitosan (CS) and gum arabic (GA). Materials and Methods: Ciprofloxacin (CPX) was administered orally to adult male Wistar albino rats at a dose of 50 mg/kg for 14 days to induce depression. Clomipramine HCl solution and the drug-loaded nano complexes (NC) were administrated for 14 days via the oral route (50 mg/kg) and intranasal route (500 µg/kg). Results: All the prepared drug-loaded nano-complexes (NC) were uniformly distributed (PDI ˂0.2), NC1 (composed of CS:GA 1:1) attained the smallest particle size (200.30 ± 26.07nm) and the most sustained release profile (Mean Release Time= 96.02± 8.36 min.) and has a spherical outline as detected by transmission electron microscope. Treatment with clomipramine-loaded NC via oral and intranasal routes elevated swimming time, serotonin (5-HT), excitatory amino acid transporter 2 (EAAT2) and Gamma-aminobutyric acid (GABA) brain contents, decreased brain content of malondialdehyde (MDA) and nitric oxide (NO), and ameliorated nuclear pyknosis and degeneration of neurons compared to CPX and clomipramine solution. Clomipramine-loaded NC via intranasal routes returned the brain content of 5-HT and EAAT 2 to its normal level and has effect superior than oral route.Conclusion: Clomipramine-loaded NC administered via intranasal route showed an enhanced effect and a higher antidepressant activity than the traditional oral route through alleviating CPX neurological toxicity.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Depression, Ciprofloxacin, clomipramine, nanocomplex, chitosan, gum arabic, GAPA/EAAT2</keyword>
				<start_page>55</start_page>
				<end_page>64</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27112.html</web_url>
			<author_list><author>
				<first_name>Abeer</first_name>
				<middle_name></middle_name>
				<last_name>Salama</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>berrotec@yahoo.com</email>
				<code>119038</code>
				<coreauthor>No</coreauthor>
				<affiliation>Pharmacology Department, National Research Centre, El-Bohooth Street (P.O. 12622), Cairo, Egypt</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Rabab</first_name>
				<middle_name></middle_name>
				<last_name>Kamel</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>drrababk@hotmail.com</email>
				<code>119039</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Pharmaceutical Technology Department, National Research Centre, El-Bohooth Street, Cairo, Egypt</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Nourina</first_name>
				<middle_name></middle_name>
				<last_name>N. Ghoneim</last_name>
				<suffix></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>119040</code>
				<coreauthor>No</coreauthor>
				<affiliation>Egyptian Drug Authority, Cairo, Egypt</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Shereen</first_name>
				<middle_name></middle_name>
				<last_name>S. Elshaer</last_name>
				<suffix></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>119041</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biochemistry, Faculty of Pharmacy, Heliopolis University,Cairo,Egypt|Department of Biochemistry and Molecular Biology, Faculty of Pharmacy (Girls), Al-Azhar University, Cairo, Egypt</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Amarogentin relieves cholestatic liver injury caused by ANIT in rats by regulating the FXR and Nrf2 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): Cholestasis, a hepatic disorder characterized by impaired bile secretion, drives progressive liver damage, fibrosis, failure, and even death. This study explores how amarogentin (AG) ameliorates cholestatic liver injury in rats induced by α-naphthylisothiocyanate (ANIT).Materials and Methods: The bile flow rate, a visual indicator of the degree of intrahepatic cholestasis, was measured to assess the model’s success. Liver function was evaluated by analyzing the serum levels of enzymes (ALP, ALT, AST, TBIL, DBIL, and TBA), as well as indicators of oxidative damage (SOD, MDA, and GSH-Px), in the liver tissue, and by examining liver histopathology. Additionally, Western blot analysis was utilized to assess the protein levels of the FXR and Nrf2 signaling pathways in the liver tissue of cholestatic rats both before and after AG treatment, to understand the underlying protective mechanism.Results: AG was administered intragastrically to ANIT-treated cholestatic rats, which significantly decreased the plasma concentrations of AST, ALT, ALP, TBIL, DBIL, and TBA, and alleviated ANIT-induced liver injury. AG could also significantly improve the bile flow rate and suppress oxidative stress. Western blot analysis revealed that AG could enhance ANIT-induced cholestasis by modulating the anti-oxidative system via activation of the PI3K/Akt/Nrf2 pathway and by regulating bile acid metabolism.Conclusion: This study demonstrated that AG may mitigate ANIT-induced cholestatic liver damage by improving the bile flow rates, decreasing the concentrations of liver function markers and serum enzyme levels, enhancing liver histology, activating Nrf2 via the PI3K/Akt signaling pathway, and controlling bile acid transport.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>α-Naphthylisothiocyanate, Amarogentin, cholestasis, FXR, Mechanism, Nrf2</keyword>
				<start_page>65</start_page>
				<end_page>73</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26947.html</web_url>
			<author_list><author>
				<first_name>Wenxiang</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>wangwenxiang@cqtgmc.edu.cn</email>
				<code>118297</code>
				<coreauthor>No</coreauthor>
				<affiliation>Chongqing Three Gorges Medical College, Chongqing 404120, China|Chongqing Key Laboratory of Development and Utilization of Genuine Medicinal Materials in Three Gorges Reservoir Area, Chongqing 404120, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Wei</first_name>
				<middle_name></middle_name>
				<last_name>Xiong</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>xiongweichn202202@163.com</email>
				<code>118298</code>
				<coreauthor>No</coreauthor>
				<affiliation>Chongqing Three Gorges Medical College, Chongqing 404120, China|Chongqing Key Laboratory of Development and Utilization of Genuine Medicinal Materials in Three Gorges Reservoir Area, Chongqing 404120, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jingxin</first_name>
				<middle_name></middle_name>
				<last_name>Mao</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>2230040@cqmpc.edu.cn</email>
				<code>118299</code>
				<coreauthor>No</coreauthor>
				<affiliation>Chongqing Medical and Pharmaceutical College, Chongqing 401331, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Chunyu</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>chenchunyu@cqtgmc.edu.cn</email>
				<code>118300</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Chongqing Three Gorges Medical College, Chongqing 404120, China|Chongqing Key Laboratory of Development and Utilization of Genuine Medicinal Materials in Three Gorges Reservoir Area, Chongqing 404120, 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>Evaluation of cytotoxic, anti-oxidant, and apoptotic effects of Dysphania botrys extract on B16F10 and MCF-7 cell lines</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): Dysphania botrys (L.) Mosyakin &amp; Clemants (Basionym: Chenopodium botrys L.), belonging to the Amaranthaceae family, has been used for the treatment of inflammation, bacterial and viral infections, and diabetes. In this study, we aimed to evaluate the potential cytotoxic, anti-oxidant, and apoptotic activities of methanol (MeOH) extract and petroleum ether (PE) and dichloromethane (DCM) fractions of D. botrys against B16F10 and MCF-7 cell lines. Materials and Methods: The anti-oxidant activities of fractions were measured using FRAP, DPPH, and β-carotene assays. The cytotoxicity of extracts and the intracellular ROS content were assessed using resazurin and DCFH-DA assays, respectively. A flow cytometry assay using PI staining was performed to measure the apoptotic activity of the fractions. Total phenolic and flavonoid content was determined using spectrophotometric methods. Results: The DCM fraction of D. botrys exhibited the highest anti-oxidant activity in FRAP, DPPH, and β-carotene assays, which also showed the highest amount of phenolic and flavonoid content compared to the MeOH extract and PE fraction. Cell viability and intracellular ROS content were significantly decreased following the treatment of B16F10 and MCF-7 cells with 100 and 200 µg/ml DCM and PE fractions. Treatment with 200 µg/ml DCM and PE fractions increased apoptosis in B16F10 cells. Conclusion: DCM fraction of D. botrys had significant anti-oxidant effects that may be associated with its phenolic and flavonoid compounds. It seems that terpenoid compounds are responsible for cytotoxic effects. Hence, complementary studies are needed to assess other bioactive compounds of D. botrys and their protective mechanisms.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Amaranthaceae, Anti-oxidant, Apoptosis, Cytotoxicity, Dysphania botrys, Flavonoid content, Phenolic content</keyword>
				<start_page>74</start_page>
				<end_page>80</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27021.html</web_url>
			<author_list><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Forouzanfar</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>forouzanfarf@mums.ac.ir</email>
				<code>118625</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran|Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>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>el.ramazani@yazd.ac.ir</email>
				<code>118626</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, Yazd University, Yazd, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad</first_name>
				<middle_name></middle_name>
				<last_name>Esmaeili</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>esmaelisanim941@mums.ac.ir</email>
				<code>118627</code>
				<coreauthor>No</coreauthor>
				<affiliation>Medical Toxicology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seyed Ahmad</first_name>
				<middle_name></middle_name>
				<last_name>Emami</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>emamia@mums.ac.ir</email>
				<code>118628</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Traditional Pharmacy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>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>118629</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>18β-Glycyrrhetinic acid-loaded silver nanoparticles mitigate neuroinflammation and endoplasmic reticulum stress in the brain tissue of diabetic rats</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Diabetes mellitus (DM) causes oxidative stress, neuroinflammation, and endoplasmic reticulum (ER) dysfunction that contribute to neurodegeneration. This study investigated the effects of 18β-glycyrrhetinic acid-loaded silver nanoparticles (18β-GA-AgNPs) on brain injury in diabetic rats. Materials and Methods: Fifty-six male Wistar rats were divided into eight groups: Sham, 18β-GA, AgNPs, 18β-GA-AgNPs, DM, DM+18β-GA, DM+AgNPs, and DM+18β-GA-AgNPs. Diabetes was induced by alloxan (120 mg/kg, IP), and treatments were administered orally for 14 days. Biochemical markers (MDA, GSH, SOD), histopathology, and expression of ER stress and apoptotic proteins (ATF6, IRE1, Caspase-3, BCL-2, CREB, TNF-α, and IL-1β) were evaluated. Results: The DM group exhibited significant increases in MDA, TNF-α, IL-1β, ATF6, and Caspase-3 with reduced GSH, SOD, and BCL-2, indicating oxidative stress, inflammation, apoptosis, and ER stress. In contrast, IRE1 levels remained unchanged in DM rats but showed a slight elevation in the AgNPs group. Treatment with 18β-GA-AgNPs markedly reduced MDA, TNF-α, IL-1β, ATF6, and Caspase-3, while restoring GSH, SOD, BCL-2, and CREB expression. Histopathological analysis confirmed neuronal apoptosis and perivascular and extracellular space enlargement in DM rats, whereas 18β-GA-AgNPs substantially attenuated these changes. Overall, 18β-GA-AgNPs provided synergistic neuroprotection by suppressing oxidative stress, inflammation, and ER stress while enhancing antioxidant and anti-apoptotic defenses. Conclusion: These findings suggest that 18β-GA-AgNPs may represent a promising therapeutic strategy against diabetes-associated neurodegeneration, although further long-term, ultrastructural, and sex-inclusive studies are warranted.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Apoptosis, Brain, Diabetes Mellitus, Endoplasmic reticulum - stress, Glycyrrhetinic acid, Neuroinflammation, Oxidative stress, Silver nanoparticles</keyword>
				<start_page>81</start_page>
				<end_page>89</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27029.html</web_url>
			<author_list><author>
				<first_name>Seçil Nazife</first_name>
				<middle_name></middle_name>
				<last_name>Parlak</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>seeparlak@gmail.com</email>
				<code>118662</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Medicine, Ağrı İbrahim Çeçen University, Agri, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seda</first_name>
				<middle_name></middle_name>
				<last_name>Yakut</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sedaayakut@gmail.com</email>
				<code>118663</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Veterinary Medicine, Mehmet Akif Ersoy University, Burdur, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Adem</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>adem.kara@erzurum.edu.tr</email>
				<code>118664</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Özlem</first_name>
				<middle_name></middle_name>
				<last_name>Demir</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ozlem.abuc@erzincan.edu.tr</email>
				<code>118665</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Turkey</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Saime</first_name>
				<middle_name></middle_name>
				<last_name>Özbek Şebin</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>saime.ozbek@atauni.edu.tr</email>
				<code>118666</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, Faculty of Medicine, Atatürk University, Erzurum, 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>Parthenolide attenuated the endometriosis-like lesions by activating autophagy and suppressing NLRP3 inflammasome activity</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): Parthenolide (PTL) has significant anti-inflammatory and immunomodulatory effects, but its regulatory mechanisms in endometriosis (EMs) remain unclear. This study aimed to systematically evaluate the effects of PTL on cellular models and a murine EMs model, with a focus on its regulatory roles in autophagy and the NLRP3 inflammasome pathway.Materials and Methods: Human monocytic leukemia THP-1 cells, murine immortalized bone marrow-derived macrophages, and 30 female C57BL/6 mice were used. Autophagy-related proteins (Beclin1, LC3, p62) and inflammasome components (NLRP3, ASC, caspase-1) were detected by Western blotting, and the activation of the AMPK/ULK1 signaling pathway was assessed after treating with PTL at a concentration of 10 mg/ml for 1 hr. A murine EMs model was established by peritoneal implantation, followed by intraperitoneal injections of PTL (10 mg/ml). Immunohistochemical staining was performed to detect the expression of NLRP3, caspase-1, IL-1β, and GSDMD in ectopic lesions.Results: In vitro, PTL (10 mg/ml) significantly inhibited the activation of NLRP3, caspase-1-p20, IL-1β, and GSDMD, while increasing the phosphorylation levels of Beclin1 and AMPK/ULK1, and decreasing the expression of p62 and LC3, indicating enhanced autophagic flux. In vivo, PTL treatment markedly reduced the number, surface area, and weight of ectopic lesions in mice, and significantly suppressed the expression of inflammatory proteins in the lesions.Conclusion: PTL exerts its therapeutic effect on EMs by simultaneously activating autophagy through the AMPK/ULK1 signaling pathway and inhibiting the NLRP3 inflammasome and its downstream effectors.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Autophagic, Endometriosis, Inflammasomes, Inflammatory response, NLRP3 protein, Parthenolide</keyword>
				<start_page>90</start_page>
				<end_page>100</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26995.html</web_url>
			<author_list><author>
				<first_name>Luhongyuan</first_name>
				<middle_name></middle_name>
				<last_name>Jin</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>jlhy510@outlook.com</email>
				<code>118499</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Gynecology and Obstetrics, The Fourth Affiliated Hospital of Soochow University, Suzhou 215000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Tingting</first_name>
				<middle_name></middle_name>
				<last_name>Fu</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ft18875210696@163.com</email>
				<code>118500</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Orthopedics, The Fourth Affiliated Hospital of Soochow University, Suzhou 215000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Chi</first_name>
				<middle_name></middle_name>
				<last_name>Chi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>chichi17610@163.com</email>
				<code>118501</code>
				<coreauthor>No</coreauthor>
				<affiliation>Nanjing University of Chinese Medicine, Nanjing 210003, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jiayi</first_name>
				<middle_name></middle_name>
				<last_name>Zhou</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>zhoujiayiom@163.com</email>
				<code>118502</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Gynecology and Obstetrics, The Fourth Affiliated Hospital of Soochow University, Suzhou 215000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jun</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>linjun@suda.edu.cn</email>
				<code>118503</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Orthopedics, The Fourth Affiliated Hospital of Soochow University, Suzhou 215000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Wenjie</first_name>
				<middle_name></middle_name>
				<last_name>Hou</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>wjhou@suda.edu.cn</email>
				<code>118504</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Gynecology and Obstetrics, The Fourth Affiliated Hospital of Soochow University, Suzhou 215000, 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>Fabrication and analysis of a PVP-carboxymethyl chitosan/forsterite nanocomposite scaffold with stainless steel base via freeze-drying and neural network techniques</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 design and fabricate innovative polymer-ceramic-metal scaffolds for bone tissue engineering, utilizing 3D printing and freeze-drying techniques to enhance bone repair.Materials and Methods: Stainless steel scaffolds were produced via selective laser melting (SLM) and coated with varying weight percentages (0, 5, 10, 15) of polyvinylpyrrolidone (PVP), carboxymethyl chitosan (CMC), and forsterite using freeze-drying. The scaffolds were characterized through Fourier transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), and scanning electron microscopy (SEM) to assess functional groups, phase purity, porosity, and pore size. Biological assessments included bioactivity, ion emission tests (ICP-AES), and wettability evaluations. Artificial neural networks (ANN) were employed to predict mechanical and biological properties. Results: The analysis revealed that scaffolds with 15% forsterite exhibited optimal mechanical and biological performance, enhancing the scaffold’s potential for clinical applications in bone repair.Conclusion: This study introduces a novel scaffold design that significantly improves bone tissue regeneration processes. The integration of advanced materials and predictive modeling through ANN paves the way for future research in the field of bone tissue engineering.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>3D printer, Artificial neural network, Bone scaffold, Forsterite, Nanoparticles</keyword>
				<start_page>101</start_page>
				<end_page>112</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27109.html</web_url>
			<author_list><author>
				<first_name>Negin</first_name>
				<middle_name></middle_name>
				<last_name>Ghanbari</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>negin.ghanbari@iau.ir</email>
				<code>119014</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Chemical Engineering, Shi.C., Islamic Azad University, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Bahareh</first_name>
				<middle_name></middle_name>
				<last_name>Kamyab Moghadas</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>kamyab.bahareh@iau.ac.ir</email>
				<code>119015</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Chemical Engineering, Shi.C., Islamic Azad University, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fereshteh</first_name>
				<middle_name></middle_name>
				<last_name>Samadi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>fereshtehsamadi12@srbiau.ac.ir</email>
				<code>119016</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Chemical Engineering, Shi.C., Islamic Azad University, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Amirsalar</first_name>
				<middle_name></middle_name>
				<last_name>Khandan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>amir_salar_khandan@yahoo.com</email>
				<code>119017</code>
				<coreauthor>No</coreauthor>
				<affiliation>2 Dental Research Center, Dental Research Institute, School of Dentistry, 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>The effect of tert-butylhydroquinone on anxiolytic- and antidepressant-like behaviors induced by post-traumatic stress disorder: A behavioral and molecular 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): Post-traumatic stress disorder (PTSD) is a crippling mental illness that commonly co-occurs with anxiety and depression. Recent studies have established a link between neuroinflammation and the development of PTSD. Studies have revealed that tert-butylhydroquinone (tBHQ) exhibits anti-inflammatory effects. This research investigated the impact of tBHQ on the amelioration of PTSD-induced depression- and anxiety-like behaviors with respect to amygdala and hippocampal MAO-A, MAO-B, IL-6, IL-10, and glucocorticoid receptor in rats. Materials and Methods: PTSD was triggered through the use of Single Prolonged Stress (SPS). The Elevated Plus Maze (EPM) and Forced Swim Test (FST) were employed to evaluate anxiety and depression, respectively. Protein assessment utilized Western blot assay for IL-6, IL-10, and the glucocorticoid receptor, in addition to enzyme-linked immunosorbent assay (ELISA) for MAO-A and MAO-B. Results: The data demonstrated that treatment with tBHQ ameliorates the depression- and anxiety-like behaviors in rats with PTSD. The ELISA findings indicated a rise in both MAO-A and B proteins in the hippocampus and amygdala due to PTSD, which was counteracted by a subthreshold amount of tBHQ. Additionally, the Western blot assay techniques revealed that PTSD led to an elevation in IL-6 levels, a pro-inflammatory cytokine, and a reduction in IL-10 levels, along with a decrease in glucocorticoid receptor expression in both brain regions, which was also counteracted by a subthreshold amount of tBHQ. Conclusion: These findings suggested that the beneficial effect of tBHQ on anxiety and depression induced by PTSD through hippocampal and amygdala MAO-A, MAO-B, IL-6, and IL-10, and glucocorticoid receptor.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Anxiety, Depression, Neuroinflammation, Post-traumatic stress - disorder (PTSD), Tert-butylhydroquinone (tBHQ)</keyword>
				<start_page>113</start_page>
				<end_page>120</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27110.html</web_url>
			<author_list><author>
				<first_name>Samaneh</first_name>
				<middle_name></middle_name>
				<last_name>Nabavi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>samaneh_nabavi@yahoo.com</email>
				<code>119019</code>
				<coreauthor>No</coreauthor>
				<affiliation>Institute for Cognitive Science Studies, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad Reza</first_name>
				<middle_name></middle_name>
				<last_name>Zarrindast</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>zarinmr@ams.ac.ir</email>
				<code>119020</code>
				<coreauthor>No</coreauthor>
				<affiliation>Institute for Cognitive Science Studies, Tehran, Iran|Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fariba</first_name>
				<middle_name></middle_name>
				<last_name>Khodagholi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>khodagholi@sbmu.ac.ir</email>
				<code>119021</code>
				<coreauthor>No</coreauthor>
				<affiliation>Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad</first_name>
				<middle_name></middle_name>
				<last_name>Nasehi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mo58na@yahoo.com</email>
				<code>119018</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Cognitive and Neuroscience Research Center, Tehran Medical Sciences, Islamic Azad University, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Solmaz</first_name>
				<middle_name></middle_name>
				<last_name>Khalifeh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>soolmaz25kh@yahoo.com</email>
				<code>119022</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, Tehran Medical Sciences, 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>Cinnamophilin ameliorates testosterone-induced prostatic hyperplasia and fibrosis by regulating 5α-reductase and TGF-β/Smad 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): Androgen and TGF-β1/Smad signaling pathways play important roles in epithelial-mesenchymal transition (EMT), fibrosis, and the development of benign prostatic hyperplasia (BPH). Cinnamophilin is extracted from Cinnamomum philippinense. The anti-proliferative and anti-fibrosis effects of cinnamophilin on the prostate remain unclear. This study aimed to investigate the therapeutic effects and molecular mechanism of action of cinnamophilin on prostate growth in testosterone propionate (TP)-treated mice.Materials and Methods: The study was conducted both in vivo and in vitro. TP was injected subcutaneously to induce prostate enlargement and growth. Cinnamophilin (40 mg/kg) was orally administered once a day in TP (7.5 mg/ kg)-treated mice for 28 days. The morphological characteristics and fibrosis of the prostate were examined by H&amp;E (Hematoxylin and Eosin) and Masson’s trichrome stain. Protein expression was determined by Western blot. BPH-1 and WPMY-1 cells were treated with different concentrations of cinnamophilin (1–100 μM). Results: Cinnamophilin (40 mg/kg) significantly reduced prostate weight and prostate index in animal models. Cinnamophilin inhibited the protein expression of 5α-reductase type II and prostate-specific antigen (PSA) in TP-treated mice. Cinnamophilin reversed morphological changes, EMT, and fibrosis in TP-treated mice. Cinnamophilin increased E-cadherin but decreased N-cadherin, vimentin, fibronectin, α-SMA, TGFBR2, TGF-β1, p-Smad2/3, collagen I, collagen III, and collagen IV protein expressions. The expression of Smad2/3 was not significantly different among these groups. Cinnamophilin (100 μM) inhibited proliferation at 48 hr in BPH-1 and WPMY-1 cells. Conclusion: These findings suggest that cinnamophilin inhibits prostate growth and mitigates EMT and fibrosis by regulating TGFβ/Smad signaling pathways. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Cinnamophilin, EMT, Fibrosis, Prostate hyperplasia, Smad, TGF-β</keyword>
				<start_page>121</start_page>
				<end_page>127</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27111.html</web_url>
			<author_list><author>
				<first_name>Di</first_name>
				<middle_name></middle_name>
				<last_name>Han</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>3092542191@qq.com</email>
				<code>119023</code>
				<coreauthor>No</coreauthor>
				<affiliation>College of Basic Medical Sciences, Yichun University, Yichun, Jiangxi Province 336000, China|College of Chemistry and Bio-engineering, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Chung-Yi</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>xx377@fy.edu.tw</email>
				<code>119024</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Medical and Health Sciences, Fooyin University, Daliao, Kaohsiung 83102, Taiwan</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>XiangPeng</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>1958551338@qq.com</email>
				<code>119025</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Clinical Medicine, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yi</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>2903775660@qq.com</email>
				<code>119026</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Clinical Medicine, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hui</first_name>
				<middle_name></middle_name>
				<last_name>Sun</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>1451876726@qq.com</email>
				<code>119027</code>
				<coreauthor>No</coreauthor>
				<affiliation>College of Basic Medical Sciences, Yichun University, Yichun, Jiangxi Province 336000, China|College of Chemistry and Bio-engineering, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>YiDan</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>1337395871@qq.com</email>
				<code>119028</code>
				<coreauthor>No</coreauthor>
				<affiliation>College of Basic Medical Sciences, Yichun University, Yichun, Jiangxi Province 336000, China|College of Chemistry and Bio-engineering, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>ManYu</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>m18347249745@163.com</email>
				<code>119029</code>
				<coreauthor>No</coreauthor>
				<affiliation>College of Basic Medical Sciences, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>JiaYi</first_name>
				<middle_name></middle_name>
				<last_name>Cai</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>caijiayijoy@163.com</email>
				<code>119030</code>
				<coreauthor>No</coreauthor>
				<affiliation>College of Basic Medical Sciences, Yichun University, Yichun, Jiangxi Province 336000, China|College of Chemistry and Bio-engineering, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jing</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>yxhjy@outlook.com</email>
				<code>119031</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Clinical Medicine, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>WenHui</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>1659961323@qq.com</email>
				<code>119032</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Clinical Medicine, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Peng</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.1976329@163.com</email>
				<code>119033</code>
				<coreauthor>No</coreauthor>
				<affiliation>College of Basic Medical Sciences, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>ZhengPing</first_name>
				<middle_name></middle_name>
				<last_name>Wu</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>wzp_yy@163.com</email>
				<code>119034</code>
				<coreauthor>No</coreauthor>
				<affiliation>College of Basic Medical Sciences, Yichun University, Yichun, Jiangxi Province 336000, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Chi-Ming</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>beagleliu@gmail.com</email>
				<code>119035</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>College of Basic Medical Sciences, Yichun University, Yichun, Jiangxi Province 336000, 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>Preparation and characterization of decellularized bovine bone as a bioscaffold for bone tissue engineering applications</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 develop and evaluate decellularized bovine bone (DBB) scaffolds and investigate their potential to promote osteogenic differentiation when combined with Crocin and Alendronate.Materials and Methods: Bovine bone was decellularized using a combination of physical (freeze–thaw cycles, sonication), chemical (sodium dodecyl sulfate), and enzymatic (deoxyribonuclease I) treatments to preserve native bone architecture. Scaffold properties were assessed by evaluating extracellular matrix (ECM) integrity and compressive strength. Biocompatibility was confirmed through cytotoxicity and hemolysis assays. In vitro osteogenesis was analyzed using alizarin red staining and qRT-PCR (quantitative real-time polymerase chain reaction) to quantify expression of osteogenic markers RUNX2, osteocalcin, osteopontin, and osteonectin following treatment with crocin (Cr 5 mg/ml), Alendronate (ALN 1 mg/ml), and their combination (Cr/ALN 5 mg/ml).Results: DBB scaffolds-maintained ECM structure and compressive strength (14.56 ± 0.82 MPa), comparable to native bovine bone (17.86 ± 0.14 MPa). No cytotoxic or hemolytic effects were observed. Crocin, Alendronate, and Cr/ALN treatments significantly enhanced RUNX2 expression (70%, 60%, and 65%, respectively), while Osteocalcin expression increased in Cr (50%) and Cr/ALN (25%) groups. Osteopontin and osteonectin expression also rose in Cr and Cr/ALN groups, supporting enhanced osteogenic differentiation.Conclusion: Based on in vitro findings, DBB scaffolds demonstrate favorable mechanical and biological properties, and loading the scaffolds with crocin and Alendronate enhanced osteogenic differentiation and matrix mineralization, indicating potential for bone-regeneration applications. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Alendronate, Bone tissue engineering, Crocin, Decellularized bone - scaffolds, Osteogenesis</keyword>
				<start_page>128</start_page>
				<end_page>137</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_26949.html</web_url>
			<author_list><author>
				<first_name>Roya</first_name>
				<middle_name></middle_name>
				<last_name>Akbarpour</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>royarad3294@gmail.com</email>
				<code>118309</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>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>118310</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>Simin</first_name>
				<middle_name></middle_name>
				<last_name>Nazarnezhad</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>smn.nazarnezhad@gmail.com</email>
				<code>118311</code>
				<coreauthor>No</coreauthor>
				<affiliation>Metabolic Syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran|Tissue Engineering Research Group (TERG), Department of Anatomy and Cell Biology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ghasem</first_name>
				<middle_name></middle_name>
				<last_name>Abbaszadeh-Goudarzi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>abbaszadehghasem@gmail.com</email>
				<code>118312</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Medical Biotechnology, 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>The protective effect of resveratrol on lupus nephritis mice by up-regulating Sirt1</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 therapeutic effect and protective mechanism of resveratrol (Res) on mice with lupus nephritis (LN).Materials and Methods: We used Res to intervene in MRL/lpr mice and employed biochemical techniques to assess kidney function, inflammation levels, and oxidative stress. We also evaluated changes in immune function and used immunohistochemistry to assess Sirt1 protein and mRNA expression.Results: Res improved the kidney function, alleviated proteinuria, and renal pathological damage in MRL/lpr mice. Res also ameliorated spleen weight and spleen index, and inhibited urinary protein/creatinine levels. Moreover, Res inhibited the expression of circulating inflammatory factors, oxidative stress levels, and kidney cell apoptosis in MRL/lpr mice. Res effectively promoted Sirt1 protein and mRNA expression in the kidneys of MRL/lpr mice. Conclusion: Res has a protective effect on MRL/lpr mice, and its mechanism may involve activation of the Sirt1 signaling pathway.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Apoptosis, Lupus nephritis, Oxidative stress, Resveratrol, SIRT1</keyword>
				<start_page>138</start_page>
				<end_page>144</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27107.html</web_url>
			<author_list><author>
				<first_name>Yu</first_name>
				<middle_name></middle_name>
				<last_name>Zhao</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>a17757461579@126.com</email>
				<code>119001</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Rheumatology, The Second Affiliated Hospital Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, P.R. China|Department of Nephrology, Ningbo Yinzhou No.2 Hospital, Ningbo, Zhejiang Province, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yun</first_name>
				<middle_name></middle_name>
				<last_name>Cai</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>cyun2011@sina.com</email>
				<code>119002</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Nephrology, Ningbo Yinzhou No.2 Hospital, Ningbo, Zhejiang Province, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jie</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>896183921@qq.com</email>
				<code>119003</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Nephrology, Ningbo Yinzhou No.2 Hospital, Ningbo, Zhejiang Province, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yang</first_name>
				<middle_name></middle_name>
				<last_name>Xu-yan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>zaq.10plm@163.com</email>
				<code>119004</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Rheumatology, The Second Affiliated Hospital Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, P.R. China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Comparative effects of estradiol and daidzein on the expression of endometrial cancer-related genes and histopathological parameters in the uterus of ovariectomized rats</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): This study compared the effects of daidzein (DZD) and 17-β-estradiol (E2) on uterine histopathology, expression of endometrial cancer-related genes, and anti-oxidant status in ovariectomized (OVX) rats.Materials and Methods: Thirty rats were divided into five groups (n=6): Sham, OVX, OVX+E2 (10 μg/kg/day), OVX+DZD (20 mg/kg/day), and DZD-only. After 50 days of treatment, uterine tissues were analyzed for histopathological changes, mRNA expression of ERα, ERβ, PTEN, EZH2, and Ki67, and oxidative stress markers (TAC, SOD, CAT, and MDA).Results: Ovariectomy induced endometrial atrophy, significantly downregulated the expression of all target genes (ERα, ERβ, PTEN, EZH2, and Ki67), decreased SOD and CAT activity and TAC level, and increased MDA. E2 treatment reversed these changes but induced hyperplastic effects. DZD administration significantly increased CAT and SOD activity and elevated ERβ and Ki67 expression compared with the OVX group. Crucially, DZD prevented uterine atrophy without inducing hyperplasia.Conclusion: DZD demonstrated a potentially beneficial effect by improving uterine anti-oxidant capacity and preventing atrophy, but without the hyperplastic changes associated with estradiol. These findings suggest that DZD may be a safer alternative for managing hypoestrogenic conditions, warranting further investigation.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Endometrial neoplasms, Estrogens, Ovariectomy, Oxidative stress, Phytoestrogens, Rats</keyword>
				<start_page>145</start_page>
				<end_page>154</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27131.html</web_url>
			<author_list><author>
				<first_name>Vahid</first_name>
				<middle_name></middle_name>
				<last_name>Setayesh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>vahidsetayesh@yahoo.com</email>
				<code>119144</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biochemistry, School of Medicine, Shiraz University of Medical Science, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Asma</first_name>
				<middle_name></middle_name>
				<last_name>Neisy</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>asmaneisi66@gmail.com</email>
				<code>119145</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biochemistry, School of Medicine, Shiraz University of Medical Science, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Maryam</first_name>
				<middle_name></middle_name>
				<last_name>Niknam</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>niknam8892@gmail.com</email>
				<code>119146</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biochemistry, School of Medicine, Shiraz University of Medical Science, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zahra</first_name>
				<middle_name></middle_name>
				<last_name>Khoshdel</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>khoshdez37@yahoo.com</email>
				<code>119147</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biochemistry, School of Medicine, Shiraz University of Medical Science, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Farhad</first_name>
				<middle_name></middle_name>
				<last_name>Koohpeyma</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>farhadbiologist@gmail.com</email>
				<code>119148</code>
				<coreauthor>No</coreauthor>
				<affiliation>Research committee, Endocrine and Metabolism Research Center, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sanaz</first_name>
				<middle_name></middle_name>
				<last_name>Alaee</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sanaz620@gmail.com</email>
				<code>119149</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Reproductive Biology, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran|Department of Natural Sciences, West Kazakhstan Marat Ospanov Medical University, Aktobe, 030012, Kazakhstan</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Zal</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>fatemehzal@yahoo.com</email>
				<code>119150</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Biochemistry, School of Medicine, Shiraz University of Medical Science, Shiraz, Iran|Infertility Research Center, Shiraz University of Medical Sciences, Shiraz, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article>
			</articleset>
			</journal>