<?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>5</month>
				<day>1</day>
			</pubdate>
			<pubdate>
				<type>gregorian</type>
				<year>2026</year>
				<month>5</month>
				<day>1</day>
			</pubdate>
			<volume>29</volume>
			<number>5</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>Rosa damascena in exercise-induced neuroinflammation and recovery: A narrative review bridging traditional medicine and translational sports science</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[Rosa damascena (Damask rose) has long been esteemed in traditional medicine for its neurocalming, anti-inflammatory, and antioxidant properties. Recent scientific interest highlights its potential to address exercise-induced physiological and psychological stress by modulating the neuroimmune axis. This narrative review synthesizes preclinical, clinical, and ethnobotanical evidence regarding R. damascena’s effects on neuroinflammation, oxidative stress, and post-exercise recovery. It aims to elucidate mechanistic pathways, assess translational applications, and propose evidence-based strategies for incorporation into sports medicine and athlete recovery protocols. A comprehensive literature search was conducted across biomedical databases up to May 2025. Eligible studies included in vitro, in vivo, and human research examining the physiological effects of R. damascena or its constituents in the context of neuropsychology, inflammation, oxidative damage, and exercise recovery. R. damascena exhibits multi-modal effects, including down-regulation of pro-inflammatory cytokines, attenuation of oxidative biomarkers, enhancement of parasympathetic activity, and modulation of serotonergic and GABAergic systems. Evidence supports its role in improving sleep quality, mood regulation, and cognitive function factors critical to athlete performance and resilience. Both preclinical and early-phase human studies indicate potential benefits in reducing delayed-onset muscle soreness (DOMS), accelerating recovery, and supporting autonomic balance. A translational framework is proposed to guide future applications and clinical trials. With its unique blend of neuroprotective, immunomodulatory, and adaptogenic properties, R. damascena presents a promising phytotherapeutic agent for exercise recovery. Bridging ancient medical traditions and modern sports science, it warrants further interdisciplinary investigation to validate its efficacy, determine optimal formulations, and ensure safety in diverse athletic populations.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Exercise, Neuroinflammation, Oxidative stress, Phytotherapy, recovery of function, Rosa damascena, Traditional Medicine</keyword>
				<start_page>641</start_page>
				<end_page>656</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27520.html</web_url>
			<author_list><author>
				<first_name>Babak</first_name>
				<middle_name></middle_name>
				<last_name>Hooshmand-Moghadam</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>b.hooshmand@um.ac.ir</email>
				<code>120850</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Exercise Physiology, Faculty of Sport Sciences, Ferdowsi University of Mashhad, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Abbas Ali</first_name>
				<middle_name></middle_name>
				<last_name>Gaeini</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>aagaeini@ut.ac.ir</email>
				<code>120851</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Exercise Physiology, Faculty of Sports and Health Sciences, University of Tehran, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Recent advances in the detection and treatment of hydatid cysts by nanomaterial-based carriers</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[Cystic echinococcosis (CE) is a neglected parasitic disease. Although several therapeutic approaches are available for CE, including PAIR (Puncture, Aspiration, Injection, Re-aspiration), surgery, chemotherapy with anthelmintic drugs, and waiting for inactive cysts, these methods face challenges, and treatment choices remain debated. Regarding chemotherapy, especially with albendazole (ABZ) as the first-line drug, efficacy is limited by poor solubility and low bioavailability. Recently, nanoparticle (NP)-based systems, or nanocarriers, have attracted much interest in drug delivery, with ABZ as the main focus. This review summarizes the latest progress in developing diverse nanocarrier systems, such as liposomes, polymeric NPs (PNPs), and metallic NPs, highlighting their potential for scolicidal activity and for improving therapeutic approaches for CE. In addition, diagnostic methods, including imaging techniques and serological tests, as well as emerging nanotechnology-based approaches such as biosensors and nanosensors, are briefly discussed to provide a more comprehensive perspective on CE management. Subsequently, the prospects and challenges of drug-loaded nanocarriers for the treatment of CE are briefly discussed to further encourage their use as a means to improve drug delivery performance in CE therapy. ]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Albendazole (ABZ), Cystic Echinococcosis, Drug Delivery, Hydatid Cyst, Nanocarriers, Nanoparticle</keyword>
				<start_page>657</start_page>
				<end_page>674</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27515.html</web_url>
			<author_list><author>
				<first_name>Nozhat</first_name>
				<middle_name></middle_name>
				<last_name>Zebardast</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>nszebardast@gmail.com</email>
				<code>120822</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Cellular and Molecular Research Center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Farid</first_name>
				<middle_name></middle_name>
				<last_name>Ajori</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>faridajory@gmail.com</email>
				<code>120823</code>
				<coreauthor>No</coreauthor>
				<affiliation>Student Research Committee, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran|Department of Parasitology, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Rahim</first_name>
				<middle_name></middle_name>
				<last_name>Nosrati</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>rahim_nosrati@gums.ac.ir</email>
				<code>120824</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Cellular and Molecular Research Center, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran|Student Research Committee, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Kurarinone: From chemistry to pharmacological values–A review</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Review Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Kurarinone (KRN) is a major prenylated flavanone isolated from Sophora flavescens, widely recognized for its diverse pharmacological activities and growing therapeutic relevance. This review provides a comprehensive and updated overview of KRN, encompassing its botanical occurrence, phytochemical characteristics, structural elucidation, and biotransformation pathways, alongside in-depth analyses of its pharmacological activities, molecular mechanisms, and pharmacokinetic behavior across experimental models. A structured literature search was conducted across PubMed, Scopus, Web of Science, and Google Scholar using the keywords “Kurarinone,” “Sophora flavescens flavonoids,” “prenylated flavanones,” and related terms. Studies reporting natural occurrence, chemical isolation, biotransformation, physicochemical properties, pharmacological mechanisms, pharmacokinetics, and toxicity were included. In vitro and in vivo experimental studies and clinical disease models were prioritized, while non-primary sources and incomplete reports were excluded. KRN exhibited a broad pharmacological profile, including anticancer, anti-inflammatory, antibacterial, antiviral, and organ-protective effects, driven by its capacity to orchestrate multiple signaling networks. Mechanistically, KRN regulated pivotal molecular pathways, such as NF-κB, MAPK, JAK2/STAT3, PI3K/Akt, Nrf2/HO-1, and caspase-dependent apoptosis, thereby modulating inflammatory responses, oxidative stress, and cell apoptosis. Biotransformation studies reveal rapid conversion into glucuronide and hydroxyl conjugates. pharmacokinetic evidence indicated poor oral bioavailability (less than 50%), extensive Phase II metabolism, and tissue-specific accumulation, particularly in hepatic compartments. While these characteristics may contribute to therapeutic action, dose-dependent hepatotoxicity has been reported, highlighting critical translational challenges and the need for formulation advances and safety optimization. Future research should emphasize pharmacokinetic-pharmacodynamic modeling, nano-delivery systems, toxicity profiling, and well-designed clinical studies to support its translational development.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Kurarinone, Molecular mechanism, Sophora flavescens, Pharmacokinetics, Pharmacology, Phytochemistry</keyword>
				<start_page>675</start_page>
				<end_page>687</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27572.html</web_url>
			<author_list><author>
				<first_name>Vu</first_name>
				<middle_name></middle_name>
				<last_name>Huy Dinh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>vuhuydinh@vnuf.edu.vn</email>
				<code>121104</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Chemistry, Vietnam National University of Forestry, Xuan Mai, Hanoi 10000, Vietnam</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ni</first_name>
				<middle_name></middle_name>
				<last_name>Huynh Thi Ngoc</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ni.huynhthingoc@htu.edu.vn</email>
				<code>121105</code>
				<coreauthor>No</coreauthor>
				<affiliation>Faculty of Education, Ha Tinh University, Cam Binh, Hatinh 480000, Vietnam</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Thuy</first_name>
				<middle_name></middle_name>
				<last_name>Tran Thi Thanh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>thuyttt@vnuf.edu.vn</email>
				<code>121106</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Chemistry, Vietnam National University of Forestry, Xuan Mai, Hanoi 10000, Vietnam</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Son</first_name>
				<middle_name></middle_name>
				<last_name>Ninh The</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>yamantson@gmail.com</email>
				<code>121107</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Institute of Chemistry, Vietnam Academy of Science and Technology (VAST), 18 Hoang Quoc Viet, Nghia Do, Hanoi 10000, Vietnam</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>Digital immune twins and ai-integrated multi-omic biomarkers: Redefining personalized immunotherapy in non-small cell lung cancer</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[Non-small cell lung cancer (NSCLC) remains one of the leading causes of global cancer mortality despite advances in immunotherapy. While immune checkpoint inhibitors (ICIs) targeting the PD-1/PD-L1 axis have transformed clinical outcomes for selected patients, response rates remain highly variable due to tumor heterogeneity, immune escape mechanisms, and evolving biomarker complexity. The need for dynamic, integrative biomarkers that better predict treatment response and guide personalized therapy is increasingly critical. This narrative review synthesizes recent advances (2023–2025) in genomic, transcriptomic, proteomic, metabolomic, and liquid-biopsy-based biomarkers relevant to NSCLC immunotherapy. Key databases, including PubMed, Scopus, and Web of Science, were screened, with emphasis on emerging artificial intelligence (AI) and digital twin–based frameworks supporting precision immuno-oncology. Across studies, single biomarkers such as PD-L1 or tumor mutational burden (TMB) demonstrate limited standalone predictive value. Multi-omic signatures incorporating circulating tumor DNA (ctDNA) fragmentomics, exosomal PD-L1, T-cell receptor (TCR) repertoire diversity, DDR alterations, metabolic checkpoint activity, and spatial immune profiling demonstrate improved accuracy and clinical relevance (clinical and preclinical evidence). AI-based multimodal models and digital immune twins further enhance predictive capacity by mapping resistance trajectories and simulating individualized therapeutic responses (computational/model-based evidence).The transition from static biomarkers toward integrated multi-omic and AI-driven decision frameworks represents a paradigm shift in NSCLC immunotherapy. These emerging platforms support a future of adaptive, anticipatory, and personalized treatment strategies with strong translational potential.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Artificial intelligence, Biomarkers, Carcinoma, Digital twins, Immunotherapy, Non-Small-Cell Lung, Precision Medicine, Programmed cell death- ligand 1</keyword>
				<start_page>688</start_page>
				<end_page>716</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27577.html</web_url>
			<author_list><author>
				<first_name>Qamar</first_name>
				<middle_name></middle_name>
				<last_name>Abuhassan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>qamarabuhassanphd@gmail.com</email>
				<code>121135</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmaceutics and Pharmaceutical Technology, School of Pharmacy, University of Jordan, Amman, 11942, Jordan</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hamzeh</first_name>
				<middle_name></middle_name>
				<last_name>Alameer</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>hamzehj.alameer.2000@gmail.com</email>
				<code>121136</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Faculty of Allied Medical Sciences, Hourani Center for Applied Scientific Research, Al-Ahliyya Amman University, Amman, Jordan</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zoltan</first_name>
				<middle_name></middle_name>
				<last_name>Balogh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>zbalogh@ukf.sk</email>
				<code>121137</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Informatics, Constantine the Philosopher University in Nitra, Tr. A. Hlinku 1, 949 01 Nitra, Slovakia|Kandó Kálmán Faculty of Electrical Engineering, Óbuda University 1034 Budapest, Bécsi út 94-96, Hungary</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mirle</first_name>
				<middle_name>Mahadevappa</middle_name>
				<last_name>Rekha</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mm.rekha@jainuniversity.a.cin</email>
				<code>121138</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Samir</first_name>
				<middle_name></middle_name>
				<last_name>Sahoo</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>samirsahu@soa.ac.in</email>
				<code>121139</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of General Medicine, IMS and SUM Hospital, Siksha ‘O’ Anusandhan, Bhubaneswar, Odisha-751003, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Muthiah</first_name>
				<middle_name></middle_name>
				<last_name>Bavanilatha</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>bavanilatha.biotech@sathyabama.ac.in</email>
				<code>121140</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biotechnology, Sathyabama Institute of Science and Technology, Chennai, Tamil Nadu, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Vimal</first_name>
				<middle_name></middle_name>
				<last_name>Arora</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>drvimalarora1@outlook.com</email>
				<code>121141</code>
				<coreauthor>No</coreauthor>
				<affiliation>University institute of Pharma Sciences, Chandigarh University, Mohali, Punjab, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Aashna</first_name>
				<middle_name></middle_name>
				<last_name>Sinha</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>aashna07sinha@gmail.com</email>
				<code>121142</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Applied and Life Sciences, Division of Research and Innovation, Uttaranchal University, Dehradun, Uttarakhand, India</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Alisher</first_name>
				<middle_name></middle_name>
				<last_name>Khazratov</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>botir.elov@mail.ru</email>
				<code>121143</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Oral Surgery and Dental Implantology, Samarkand State Medical University, Samarkand, Uzbekistan</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>Mitigation of sepsis-associated acute kidney injury by thymoquinone via targeting pyroptosis and attenuation of inflammation in C57BL/6 mice</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Acute kidney injury (AKI) is a severe, life-threatening complication of sepsis that often leads to renal failure. Thymoquinone, the main bioactive component of Nigella sativa, exhibits potent antioxidant and anti-inflammatory effects, protecting heart, liver, and kidney tissues in experimental studies. This study aimed to investigate the protective effects of thymoquinone on lipopolysaccharide (LPS)-induced AKI in mice by assessing oxidative stress, inflammatory mediators, pyroptosis factors, and renal function markers via modulation of oxidative stress and pyroptosis pathways.Materials and Methods: Thirty-two male C57BL/6 mice (20–25 g) were randomized into four groups: control, LPS, and two LPS groups treated with thymoquinone solubilized in Cremophor (1 or 10 mg/kg). AKI was induced by intraperitoneal injection of LPS (10 mg/kg). After 24 hr, blood samples were collected for blood urea nitrogen (BUN), cystatin C, and serum creatinine assays. Kidney homogenates were analyzed for malondialdehyde (MDA), superoxide dismutase (SOD), nitrite, interleukin-6 (IL-6), nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (NLRP3), and caspase-1 levels.Results: Thymoquinone (10 mg/kg; PO) significantly decreased BUN (P&lt;0.05), cystatin C (P&lt;0.05), and serum creatinine (P&lt;0.05) levels. It also reduced MDA concentration (P&lt;0.05) and increased SOD activity (P&lt;0.05), while nitrite levels remained unchanged. Furthermore, IL-6, NLRP3, and caspase-1 were significantly lower (for all factors, P&lt;0.05) in thymoquinone-treated mice compared to the LPS group.Conclusion: Thymoquinone effectively attenuates LPS-induced AKI, likely by reducing oxidative stress, inhibiting pyroptosis and inflammation, and enhancing antioxidant defenses.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Acute kidney injury, Inflammation, Lipopolysaccharide, Oxidative stress, Pyroptosis, Thymoquinone</keyword>
				<start_page>717</start_page>
				<end_page>723</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27600.html</web_url>
			<author_list><author>
				<first_name>Niloofar</first_name>
				<middle_name></middle_name>
				<last_name>Izadi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>niloofar.izadi71@gmail.com</email>
				<code>121231</code>
				<coreauthor>No</coreauthor>
				<affiliation>Faculty of Medicine, Shahed University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahdieh</first_name>
				<middle_name></middle_name>
				<last_name>Taheri</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>taheri.mahdieh1991@gmail.com</email>
				<code>121232</code>
				<coreauthor>No</coreauthor>
				<affiliation>Neurophysiology Research Center, Shahed University, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mehrdad</first_name>
				<middle_name></middle_name>
				<last_name>Roghani</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mehjour@yahoo.com</email>
				<code>121230</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Neurophysiology Research Center, Shahed 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>Protective effects and mechanism of chrysophanol against age-related osteoporosis in rats</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): This study aimed to investigate the protective effect and underlying mechanism of chrysophanol (CPH) on senile osteoporosis (OP) in rats. Materials and Methods: Twenty-four-month-old rats were divided into an aged OP model group and low- (10 mg/kg), medium- (20 mg/kg), and high-dose (50 mg/kg) CPH groups, with eight-month-old rats used as the control group. After 60 days of oral CPH administration, the bone mineral density (BMD), bone volume fraction (BV/TV), trabecular number (TbN), and trabecular separation (TbSp) of the femur were analysed using Micro-CT. Serum levels of bone formation markers (alkaline phosphatase, ALP; osteocalcin, OC) and bone resorption markers (type I collagen crosslinked N-telopeptide, NTX; tartrate-resistant acid phosphatase, TRACP) were determined by ELISA. Pathological changes in the femur were observed via H&amp;E staining, and the expression of p-AKT and p-mTOR proteins in bone marrow was detected by western blotting.Results: Compared with those in the control group, the bone formation marker levels, BMD, BV/TV, and TbN in the model group significantly decreased, whereas the bone resorption marker levels, TbSp, and expression levels of p-AKT and p-mTOR significantly increased, with obvious bone structure destruction. CPH treatment reversed these changes in a dose dependent manner, significantly enhanced bone formation, inhibited bone resorption, improved bone density and microstructure, and down-regulated the expression of p-AKT and p-mTOR. Conclusion: CPH can effectively improve bone density and microstructure in aged osteoporotic rats, and its bone-protective effect may be related to the inhibition of the PI3K/AKT/mTOR signaling pathway.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Aging, Bone Diseases/Metabolic, Chrysophanol, Osteoporosis, PI3K/AKT/mTOR signaling- pathway</keyword>
				<start_page>724</start_page>
				<end_page>729</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27579.html</web_url>
			<author_list><author>
				<first_name>Qing</first_name>
				<middle_name></middle_name>
				<last_name>Lu</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>1045347822@qq.com</email>
				<code>121158</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Traditional Chinese Medicine, Suzhou City Xiangcheng District Third People’s Hospital, Suzhou 215100, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Chenxi</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>18801759639@163.com</email>
				<code>121159</code>
				<coreauthor>No</coreauthor>
				<affiliation>Institute of Translational Medicine, Shanghai University, Shanghai 200444, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Lixia</first_name>
				<middle_name></middle_name>
				<last_name>Ma</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>2278662572@qq.com</email>
				<code>121160</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Traditional Chinese Medicine, Suzhou City Xiangcheng District Third People’s Hospital, Suzhou 215100, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Xiaoyao</first_name>
				<middle_name></middle_name>
				<last_name>Yu</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>1175864881@qq.com</email>
				<code>121161</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Traditional Chinese Medicine, Suzhou City Xiangcheng District Third People’s Hospital, Suzhou 215100, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Gan</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>524945966@qq.com</email>
				<code>121162</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Traditional Chinese Medicine, Suzhou City Xiangcheng District Third People’s Hospital, Suzhou 215100, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Dagui</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>dagui1106@shu.edu.cn</email>
				<code>121163</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Institute of Translational Medicine, Shanghai University, Shanghai 200444, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fusheng</first_name>
				<middle_name></middle_name>
				<last_name>Shang</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>shangmuye116688@163.com</email>
				<code>121157</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Institute of Translational Medicine, Shanghai University, Shanghai 200444, 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>Quercetin improves ESAT-6-induced pleural mesothelial cell fibrosis by activating the NRF2/HO-1 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): This study investigated the mechanism by which quercetin suppresses oxidative stress and improves fibrosis in human pleural mesothelial cells (HPMCs) induced by the Mycobacterium tuberculosis-specific antigen early secretory antigen target protein-6 (ESAT-6) by activating the Nrf2/HO-1 signaling pathway, thereby suppressing oxidative stress.Materials and Methods: An in vitro model of ESAT-6-induced HPMC fibrosis was established. The effects of various concentrations of quercetin on HPMCs were assessed using the CCK-8 assay. Markers of oxidative stress, such as superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH), were assessed. Immunofluorescence was utilized to detect levels of nuclear factor erythroid 2-related factor 2 (Nrf2), and western blot analysis was conducted to evaluate the protein levels of Nrf2, heme oxygenase-1 (HO-1), E-cadherin (E-cad), and α-smooth muscle actin (α-SMA).Results: Quercetin significantly improved ESAT-6-induced HPMC proliferation, reduced the oxidative stress marker MDA, and decreased the fibrosis marker α-SMA levels. It also promoted the translocation of Nrf2 into the nucleus in ESAT-6-induced pleural mesothelial cell fibrosis. Furthermore, quercetin enhanced the enzymatic activity of antioxidants, particularly GSH and SOD, and increased the expression levels of HO-1, Nrf2, and E-cad.Conclusion: The findings indicate that quercetin can inhibit oxidative stress by modulating the Nrf2 pathway and up-regulating HO-1 activity, thereby improving ESAT-6-induced pleural mesothelial cell fibrosis.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>ESAT-6, Fibrosis, HPMCs, Nrf2/HO-1, Quercetin</keyword>
				<start_page>730</start_page>
				<end_page>735</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27606.html</web_url>
			<author_list><author>
				<first_name>Lina</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>linachen1210@126.com</email>
				<code>121250</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Tuberculosis, Guiyang Public Health Clinical Center, Guiyang, Guizhou, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zhou</first_name>
				<middle_name></middle_name>
				<last_name>Yu</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>2590529437@qq.com</email>
				<code>121251</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China|Department of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zhuo</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>1105863089@qq.com</email>
				<code>121252</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pathology, Guiyang Public Health Clinical Center, Guiyang, Guizhou, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Bin</first_name>
				<middle_name></middle_name>
				<last_name>Tian</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>516727153@qq.com</email>
				<code>121253</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pathology, Guiyang Public Health Clinical Center, Guiyang, Guizhou, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zhongfeng</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>1017899870@qq.com</email>
				<code>121254</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Yiju</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>chengchengyiju@126.com</email>
				<code>121255</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Respiratory and Critical Care Medicine, The Fourth People’s Hospital of Guiyang, Guiyang, Guizhou, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hai</first_name>
				<middle_name></middle_name>
				<last_name>Long</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>longlong1225@126.com</email>
				<code>121256</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Infectious Diseases, Guiyang Public Health Clinical Center, Guiyang, Guizhou, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Niwen</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>huangniwen@163.com</email>
				<code>121249</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, 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>Repurposing an antimicrobial arginine-rich decapeptide as a novel anticancer agent: Evidence from in vitro and in vivo breast cancer models</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): Arginine-rich peptides have attracted interest because of their ability to interact with negatively charged cancer cell membranes. The present study aimed to evaluate the anticancer properties of a novel antimicrobial arginine-rich decapeptide (RL10) in vitro and in vivo. Materials and Methods: Cytotoxicity was assessed in breast (4T1), colon (SW480), and normal fibroblast (NIH3T3) cell lines by MTT assay following 48- and 72-hr treatment (6-400 µg/ml). Membrane integrity was examined in 4T1 cells after 48 hr using lactate dehydrogenase (LDH) release. Flow cytometry was applied to determine apoptosis induction and alterations in cell cycle distribution. Caspase 3/7 activity was also evaluated. Apoptosis-related gene expressions were analyzed using RT-PCR. The antitumor effect of RL10 was assessed in a murine 4T1 model, followed by histopathological analysis using H&amp;E staining.Results: RL10 significantly declined cancer cell viability in a dose-dependent manner, with no toxicity on normal cells. No increase in LDH release was detected. Flow cytometry revealed 28.9% apoptosis induction and cell cycle arrest at the S and G2/M phases. Marked upregulation of the Casp9 gene suggested possible activation of the intrinsic apoptotic pathway; however, Bax, Bcl2, p53, and Casp8 expressions remained unchanged. In vivo, two weeks’ treatment with the peptide suppressed tumor growth by nearly 39% (P˂0.01), accompanied by increased apoptotic figures and reduced mitotic counts. Conclusion: These findings provide the first evidence that an arginine-rich short peptide exhibits anticancer activity through apoptosis induction and tumor growth inhibition, underscoring its potential as a candidate for cancer therapy or drug delivery systems.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Antineoplastic agents, Apoptosis, Cell cycle/drug effects, Dual-function peptide, Peptides/chemistry</keyword>
				<start_page>736</start_page>
				<end_page>743</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27476.html</web_url>
			<author_list><author>
				<first_name>Reyhane</first_name>
				<middle_name></middle_name>
				<last_name>Chamani</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>chamani@yazd.ac.ir</email>
				<code>120707</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Biology, Yazd University, Yazd, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Maryam</first_name>
				<middle_name></middle_name>
				<last_name>Mohammadi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>maryammohammadi9955@gmail.com</email>
				<code>120708</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biology, Yazd University, Yazd, 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>Inhibition of the PKC-TRPV1-SP axis by propolis ameliorates chronic inflammatory pain in mice</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Chronic inflammatory pain significantly affects patient quality of life; however, existing treatment methods have limitations. Propolis is rich in various bioactive ingredients, such as flavonoids and phenolic acids. This study aimed to explore the effects and action mechanisms of propolis against chronic inflammatory pain.Materials and Methods: A mouse model of chronic inflammatory pain was established using Complete Freund’s adjuvant, with the mice divided into normal control, model, and propolis-treated groups. Body weight, pain score, foot volume, thermal pain threshold, mechanical pain threshold, and pathological changes in the toe tissue were recorded before injection (day 0) and on days 1, 7, 14, 21, and 28 after injection.After the experiment, changes in inflammatory factors (TNF-α, IL-4, IL-6, and IL-10) were detected, and the expression and distribution of proteins associated with the PKC-TRPV1-SP signalling axis in the toe, spinal cord, and hippocampus were detected by Western blot and immunofluorescence.Results: Propolis treatment significantly inhibited foot swelling, alleviated tissue inflammatory lesions, relieved pain, and increased heat and mechanical pain thresholds in mice. In addition, propolis inhibited the secretion of pro-inflammatory cytokines TNF-α, IL-4, and IL-6, promoted the secretion of the anti-inflammatory cytokine IL-10, and inhibited the expression of proteins related to the PKC-TRPV1-SP signalling axis.Conclusion: This study demonstrated that propolis exerts anti-inflammatory and analgesic effects by regulating the PKC-TRPV1-SP signalling axis. The findings offer new perspectives for the clinical treatment of chronic inflammatory pain and provide a reference for the development of new medications.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Analgesia, Anti-inflammation, chronic inflammation, Mice, Pain, Propolis</keyword>
				<start_page>744</start_page>
				<end_page>751</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27574.html</web_url>
			<author_list><author>
				<first_name>Jia-Yi</first_name>
				<middle_name></middle_name>
				<last_name>Yu</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>1263689703@qq.com</email>
				<code>121115</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Clinical Medicine, Wannan Medical College, Wuhu, 241002, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Si-Yuan</first_name>
				<middle_name></middle_name>
				<last_name>Yin</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>306646713@qq.com</email>
				<code>121116</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Medical Imageology, Wannan Medical College, Wuhu, 241002, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hui</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>3042046398@qq.com</email>
				<code>121117</code>
				<coreauthor>No</coreauthor>
				<affiliation>School of Pharmacy, Wannan Medical College, Wuhu, 241002, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Min</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>624653162@qq.com</email>
				<code>121118</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, School of Basic Medical Sciences, Wannan Medical College, Wuhu, 241002, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Juan</first_name>
				<middle_name></middle_name>
				<last_name>Dong</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>1906326049@qq.com</email>
				<code>121119</code>
				<coreauthor>No</coreauthor>
				<affiliation>Functional experiment center, School of Basic Medical Sciences, Wannan Medical College, Wuhu, 241002, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Li</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>1359388472@qq.com</email>
				<code>121120</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, School of Basic Medical Sciences, Wannan Medical College, Wuhu, 241002, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Xue-Li</first_name>
				<middle_name></middle_name>
				<last_name>Yin</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>yinxue887@163.com</email>
				<code>121121</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Functional experiment center, School of Basic Medical Sciences, Anhui Medical University, Hefei,230032, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Jing</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>247948083@qq.com</email>
				<code>121122</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Physiology, School of Basic Medical Sciences, Wannan Medical College, Wuhu, 241002, 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>Combining sorafenib and Lactobacillus rhamnosus GG reduces liver fibrosis and hepatic encephalopathy following bile duct ligation 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): Liver fibrosis can progress to hepatic encephalopathy (HE). While sorafenib is a drug employed to treat liver fibrosis, its use is linked to drug resistance and adverse effects. We examined the potential benefits of combining sorafenib with the probiotic Lactobacillus rhamnosus GG (LGG) on liver fibrosis and HE in bile duct ligated (BDL) rats. Materials and Methods: Forty male rats were randomly assigned to five groups of eight rats each, including sham, BDL, BDL+probiotic (LGG, 1×109 CFU/ml/day), BDL+sorafenib (20 mg/kg), and BDL+probiotic+sorafenib. First, rats receive probiotic LGG or solvent for 2 weeks. Following a one-week post-BDL recovery period, the animals received sorafenib and probiotic LGG for three consecutive weeks. Next, various parameters were appraised. Results: The combination of sorafenib with LGG led to less liver fibrosis when compared with sorafenib alone. This combination therapy also alleviated inflammation and oxidative species present in the liver and frontal cortex. Further, this combination diminished hepatic Toll-like receptor 4/ Nuclear factor kappa-β expression. Finally, it led to improved cognitive function in behavioral assessments compared to using sorafenib alone. Conclusion: Overall, combining a low dose of sorafenib with probiotic LGG may offer significant benefits for treating liver fibrosis and HE.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Hepatic encephalopathies, Lactobacillus Rhamnosus, Liver fibrosis, Probiotic, Sorafenib</keyword>
				<start_page>752</start_page>
				<end_page>765</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27519.html</web_url>
			<author_list><author>
				<first_name>Tina</first_name>
				<middle_name></middle_name>
				<last_name>Rahjoo</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>tinarahjoo70@gmail.com</email>
				<code>120842</code>
				<coreauthor>No</coreauthor>
				<affiliation>Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran|Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ghorbangol</first_name>
				<middle_name></middle_name>
				<last_name>Ashabi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>as_habi@yahoo.com</email>
				<code>120844</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Soheila</first_name>
				<middle_name></middle_name>
				<last_name>Adeli</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>soheilaadeli8@gmail.com</email>
				<code>120845</code>
				<coreauthor>No</coreauthor>
				<affiliation>Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Shahnaz</first_name>
				<middle_name></middle_name>
				<last_name>Halimi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>shahnazhalimi@gmail.com</email>
				<code>120846</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Microbiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mahshid</first_name>
				<middle_name></middle_name>
				<last_name>Panahi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mahshid_panahi@yahoo.com</email>
				<code>120847</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pathology, Firoozgar Hospital, Iran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Omid Reza</first_name>
				<middle_name></middle_name>
				<last_name>Tamtaji</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>tamtaji.or@gmail.com</email>
				<code>120848</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Reihaneh</first_name>
				<middle_name></middle_name>
				<last_name>Ghasemi-tarie</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>reihan.g.t@gmail.com</email>
				<code>120849</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fatemeh</first_name>
				<middle_name></middle_name>
				<last_name>Nabavizadeh</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>nabavizadeh@tums.ac.ir</email>
				<code>120843</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran|Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Cannabidiol attenuates lung ischemia-reperfusion injury by modulating RIPK1/RIPK3-mediated necroptosis and HIF-1α/VEGF signaling</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Lung ischemia-reperfusion (IR) injury is a critical clinical condition characterized by oxidative stress, inflammation, and necroptosis, often leading to severe complications. Cannabidiol (CBD), a non-psychoactive cannabinoid, has demonstrated anti-oxidant and anti-inflammatory properties, but its role in modulating lung IR injury remains incompletely understood. This study investigated the protective effects of CBD on lung IR injury in rats, focusing on the RIPK1/RIPK3 necroptosis pathway and the HIF-1α/VEGF/eNOS signaling axis.Materials and Methods: Forty male Wistar albino rats were randomized into four groups: control, IR, IR+CBD (5 mg/kg), and CBD-only. Histopathological, immunohistochemical (TNF-α, Caspase-3), biochemical (TOS, TAS, OSI), and gene expression (RIPK1, RIPK3, HIF-1α, VEGF, eNOS) analyses were performed. The IR group exhibited significant oxidative stress, inflammation, and tissue damage, with elevated TNF-α, Caspase-3, TOS, OSI, and necroptosis/apoptosis markers.Results: CBD treatment markedly attenuated these effects, reducing oxidative stress (↑TAS, ↓TOS/OSI), suppressing inflammation (↓TNF-α), and inhibiting both apoptotic (↓Caspase-3) and necroptotic (↓RIPK1/RIPK3) pathways. Additionally, CBD down-regulated HIF-1α/VEGF/eNOS expression, suggesting modulation of hypoxia-responsive signaling. Conclusion: These findings demonstrate that CBD mitigates lung IR injury by targeting oxidative stress, inflammation, and cell death mechanisms, highlighting its potential as a therapeutic agent. Further preclinical and clinical studies are warranted to validate these results.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Cannabidiol, hypoxia-Inducible factor 1, Alpha subunit, Ischemia, Lung injury, Necroptosis, Oxidative stress -reperfusion, Vascular endothelial Growth factor A</keyword>
				<start_page>766</start_page>
				<end_page>773</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27571.html</web_url>
			<author_list><author>
				<first_name>Hasan</first_name>
				<middle_name>Ekrem</middle_name>
				<last_name>Camas</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>hasancamas@sdu.edu.tr</email>
				<code>121095</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Thoracic Surgery, Faculty of Medicine, Suleyman Demirel University, Isparta, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mehtap</first_name>
				<middle_name></middle_name>
				<last_name>Savran</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mehtapsavran@sdu.edu.tr</email>
				<code>121096</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacology, Faculty of Medicine, Suleyman Demirel University, Isparta 32200, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Serap</first_name>
				<middle_name></middle_name>
				<last_name>Yildirim</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>serapolmn@gmail.com</email>
				<code>121097</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Thoracic Surgery, Faculty of Medicine, Suleyman Demirel University, Isparta, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Suleyman</first_name>
				<middle_name>Emre</middle_name>
				<last_name>Akin</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>suleymanakin@sdu.edu.tr</email>
				<code>121098</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Thoracic Surgery, Faculty of Medicine, Suleyman Demirel University, Isparta, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Rasih</first_name>
				<middle_name></middle_name>
				<last_name>Yazkan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>rasihyazkan@sdu.edu.tr</email>
				<code>121099</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Thoracic Surgery, Faculty of Medicine, Suleyman Demirel University, Isparta, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ilter</first_name>
				<middle_name></middle_name>
				<last_name>Ilhan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ilterilhan@sdu.edu.tr</email>
				<code>121100</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Biochemistry, Faculty of Medicine, Suleyman Demirel University, Isparta 32200, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Muhammet</first_name>
				<middle_name>Yusuf</middle_name>
				<last_name>Tepebasi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>muhammettepebasi@sdu.edu.tr</email>
				<code>121101</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Genetic, Faculty of Medicine, Suleyman Demirel University, Isparta 32200, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mehmet</first_name>
				<middle_name>Abdulkadir</middle_name>
				<last_name>Sevuk</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mehmetsevuk@sdu.edu.tr</email>
				<code>121102</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pharmacology, Faculty of Medicine, Suleyman Demirel University, Isparta 32200, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ozlem</first_name>
				<middle_name></middle_name>
				<last_name>Ozmen</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>ozlemoz@mehmetakif.edu.tr</email>
				<code>121103</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Pathology, Faculty of Veterinary, Burdur Mehmet Akif Ersoy University, Burdur 15000, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>CD73 blockade alleviates collagen-induced arthritis by inhibiting synovial fibroblast 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): Rheumatoid arthritis (RA) is a chronic autoimmune disease with progressive cartilage erosion and joint destruction. CD73 plays a critical role in regulating inflammatory responses. This study aims to investigate the effects of CD73 blockade on RA progression and explore the potential mechanism.Materials and Methods: Soluble CD73 levels were determined by enzyme-linked immunosorbent assay. Immunohistochemistry (IHC) was used to detect CD73 expression in tissues. A collagen-induced arthritis (CIA) rat model was used to evaluate the effect of CD73 inhibitors in vivo. Hematoxylin and eosin staining was used to evaluate synovial tissue inflammation. Safranin O/Fast Green staining and Micro-CT were used to evaluate cartilage erosion and bone destruction. A live cell imaging system was used to analyze cell proliferation. Cell invasion experiments were performed using Transwell chambers. Results: Our data showed that CD73 expression was significantly increased in synovial tissues and serum from RA patients. The increased CD73 expression may be attributed to the hypoxic microenvironment via the hypoxia-inducible factor pathway in synovial tissues. Using CIA rats, our data demonstrated that CD73 blockade alleviated bone destruction and synovial inflammation. CD73 blockade inhibited synovioblast proliferation, invasion, and pro-inflammatory cytokine production. Moreover, transcriptome analysis revealed that differentially expressed genes (DEGs) in synovioblasts induced by CD73 blockade were primarily enriched for inflammatory responses, neutrophil chemotaxis, and integrin-mediated signaling pathways.Conclusion: CD73 blockade alleviated RA disease progression by regulating the activity of synovial fibroblasts. CD73 blockade is a potential therapeutic approach for patients with RA.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Bone destruction, CD73, Rheumatoid arthritis, Synovial fibroblasts, Synovial inflammation</keyword>
				<start_page>774</start_page>
				<end_page>781</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27573.html</web_url>
			<author_list><author>
				<first_name>Xia-nan</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>wxn0427@163.com</email>
				<code>121108</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Laboratory, Tangdu Hospital, Fourth Military Medical University, Xi’an, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Rui-cheng</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>lirc16@163.com</email>
				<code>121109</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Laboratory, Tangdu Hospital, Fourth Military Medical University, Xi’an, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ruo-xuan</first_name>
				<middle_name></middle_name>
				<last_name>Hei</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>841479863@qq.com</email>
				<code>121110</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Laboratory, Tangdu Hospital, Fourth Military Medical University, Xi’an, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Chong</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>lc83832578@163.com</email>
				<code>121111</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Laboratory, Tangdu Hospital, Fourth Military Medical University, Xi’an, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zhao-wei</first_name>
				<middle_name></middle_name>
				<last_name>Gao</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>gaozhaowei1@126.com</email>
				<code>121112</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Clinical Laboratory, Tangdu Hospital, Fourth Military Medical University, Xi’an, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Xi</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>wang_xiwx@hotmail.com</email>
				<code>121113</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Clinical Laboratory, Tangdu Hospital, Fourth Military Medical University, Xi’an, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Ke</first_name>
				<middle_name></middle_name>
				<last_name>Dong</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>tdjyk3@fmmu.edu.cn</email>
				<code>121114</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Clinical Laboratory, Tangdu Hospital, Fourth Military Medical University, Xi’an, 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>Transforming PRP into a Shelf-Stable therapy: Lyophilization preserves angiogenic and regenerative properties</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): Platelet-rich plasma (PRP) is widely used in regenerative medicine due to its high concentration of bioactive growth factors; however, its short shelf life limits its clinical applicability. Lyophilization has been proposed to extend PRP stability, but its impact on biological efficacy remains unclear. This study evaluated whether lyophilization alters the biochemical composition and regenerative function of PRP derived from expired platelet units unsuitable for transfusion.Materials and Methods: Pooled isogroup PRP was processed as either liquid PRP or lyophilized PRP. Growth factors (FGF-1, PDGF, VEGF) and endotoxin levels were quantified. Biological activity was assessed in human dermal fibroblasts (HDFs) and human umbilical vein endothelial cells (HUVECs) using MTT assays, in vitro wound closure, gene expression analysis (MMP-1, MMP-3, Ang1, PDGFR), and CD31 immunocytochemistry at 5% and 10% concentrations, with fetal bovine serum (FBS) as a control.Results: Lyophilization resulted in moderate reductions in FGF-1, PDGF, and VEGF relative to Liquid-PRP (P&lt;0.05), while endotoxin levels remained acceptable. In HDFs, liquid-PRP induced higher MMP-1 and MMP-3 expression, whereas lyophilized-PRP promoted lower but sufficient expression, consistent with controlled extracellular matrix remodeling, with comparable wound-closure outcomes between PRP groups. In HUVECs, lyophilized PRP preserved cell viability, migration, and CD31 expression, comparable to liquid PRP and FBS. Angiogenic gene expression showed a concentration-dependent response, with maximal activation at 5% PRP, and no functional impairment after lyophilization (P&lt;0.05).Conclusion: Despite a moderate reduction in growth factors, lyophilized PRP retained regenerative efficacy, supporting lyophilization as a viable strategy for the stable, sustainable reuse of PRP.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Fibroblast, HUVECs, Lyophilization, Platelet-rich plasma, Regenerative medicine, Wound healing</keyword>
				<start_page>782</start_page>
				<end_page>793</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27477.html</web_url>
			<author_list><author>
				<first_name>Amin</first_name>
				<middle_name></middle_name>
				<last_name>Solouki</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>aminsolouki.h@gmail.com</email>
				<code>120709</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Tahereh</first_name>
				<middle_name></middle_name>
				<last_name>Manoochehrabadi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>manoochehrabadit68@gmail.com</email>
				<code>120710</code>
				<coreauthor>No</coreauthor>
				<affiliation>Tissue Engineering Research Group, Department of Anatomy and Cell Biology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohammad Hossein</first_name>
				<middle_name></middle_name>
				<last_name>Mohammadi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mohamad.mohamadi2@gmail.com</email>
				<code>120711</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Hamid Reza</first_name>
				<middle_name></middle_name>
				<last_name>Rahimi</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>rahimihr@mums.ac.ir</email>
				<code>120712</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Medical Genetics &amp; Molecular Medicine, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran|Medical Genetics Research Center, Mashhad University of Medical Sciences, Mashhad, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mohsen</first_name>
				<middle_name></middle_name>
				<last_name>Hamidpour</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>mohsenhp@sbmu.ac.ir</email>
				<code>120713</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Hematopoietic Stem Cell Research Centre-Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>Eugenol attenuates paclitaxel-induced cardiotoxicity by modulating autophagy-related markers 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): Paclitaxel (PTX) is a commonly used chemotherapeutic agent that causes cardiotoxicity characterized by oxidative stress, inflammation, and mitochondrial dysfunction, which disrupts autophagy and apoptosis in cardiomyocytes. This study investigated the therapeutic potential of eugenol (EUG), a natural anti-oxidant and anti-inflammatory compound, against PTX-induced cardiac damage.Materials and Methods: Thirty-six male Wistar rats were randomly assigned to six groups: Control, EUG5, EUG25, PTX, PTX+EUG5, and PTX+EUG25. Hemodynamic parameters (systolic and diastolic blood pressure and heart rate), serum cardiac biomarkers (troponin T and brain natriuretic peptide), histopathological alterations, and immunohistochemical expression of autophagy-related proteins (mTOR, ULK1, and Atg13) were evaluated.Results: PTX administration significantly reduced arterial blood pressure and increased serum cardiac injury biomarkers, accompanied by marked myocardial structural damage. Histopathological analysis revealed myocardial degeneration, inflammation, edema, and tissue disorganization in the PTX group. In PTX-exposed rats treated with EUG, arterial blood pressure was higher, and serum cardiac injury biomarkers were lower than in the PTX group, accompanied by reduced histopathological scores. PTX exposure was associated with decreased mTOR expression and increased ULK1 and Atg13 immunoreactivity, while EUG-treated PTX groups showed values closer to those of the control group for these autophagy-related markers.Conclusion: EUG administration was associated with reduced biochemical and histopathological indicators of cardiac injury in PTX-exposed rats, along with changes in autophagy-related markers. These findings demonstrate that EUG treatment coincided with attenuation of PTX-induced cardiac injury at the biochemical and histopathological levels, suggesting its potential experimental value in models of chemotherapy-associated cardiotoxicity.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Autophagy, Eugenol, Heart Injuries, Mechanistic target of - rapamycin complex 1, mTOR, Oxidative stress, Paclitaxel, Rats</keyword>
				<start_page>794</start_page>
				<end_page>803</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27555.html</web_url>
			<author_list><author>
				<first_name>Halime</first_name>
				<middle_name></middle_name>
				<last_name>Tozak Yıldız</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>htyildiz@ahievran.edu.tr</email>
				<code>120989</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Medicine, Kirsehir Ahi Evran University, 40100 Kirsehir, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Sadık</first_name>
				<middle_name></middle_name>
				<last_name>Küçükgünay</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sadik.kucukgunay@ahievran.edu.tr</email>
				<code>120990</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Medical Pharmacology, Faculty of Medicine, Kirsehir Ahi Evran University, 40100 Kirsehir, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Oya</first_name>
				<middle_name></middle_name>
				<last_name>Korkmaz</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>oya.korkmaz@ozal.edu.tr</email>
				<code>120991</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Histology and Embryology, Faculty of Medicine, Malatya Turgut Ozal University, 44210 Malatya, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Seda</first_name>
				<middle_name></middle_name>
				<last_name>Koçak</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>sdakocak@gmail.com</email>
				<code>120992</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Physiology, Faculty of Medicine, Kirsehir Ahi Evran University, 40100 Kirsehir, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Mustafa Numan</first_name>
				<middle_name></middle_name>
				<last_name>Bucak</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>bucak@selcuk.edu.tr</email>
				<code>120993</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Fertilization and Artificial Inseminatıon, Faculty of Veterinary Medicine, Selcuk University, 42250 Konya, Türkiye</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article><article>
				<language>en</language>
				<article_id_issn></article_id_issn>
				<article_id_issn_online></article_id_issn_online>
				<article_id_pubmed></article_id_pubmed>
				<article_id_pii></article_id_pii>
				<article_id_doi></article_id_doi>
				<article_id_iranmedex></article_id_iranmedex>
				<article_id_magiran></article_id_magiran>
				<article_id_sid></article_id_sid>
				<title_fa></title_fa>
				<title>HIPK2 protects neurons from oxidative stress and modulates central nervous system responses following traumatic brain injury</title>
				<subject_fa></subject_fa>
				<subject></subject>
				<content_type_fa></content_type_fa>
				<content_type>Original Article</content_type>
				<abstract_fa><![CDATA[]]></abstract_fa>
				<abstract><![CDATA[Objective(s): Traumatic brain injury (TBI) induces oxidative stress, contributing to secondary neuronal damage. This study aimed to elucidate the role of the stress-responsive kinase HIPK2 in regulating endogenous antioxidant defenses in neural tissue following TBI.Materials and Methods: We employed complementary in vitro and in vivo models: an H₂O₂-induced oxidative stress model in PC12 cells (with HIPK2 inhibited by tBID) and a controlled cortical impact mouse model of TBI (with HIPK2 overexpressed via intracerebroventricular Ad-HIPK2 injection). Analyses included assessments of cell viability, mRNA expression, and protein levels of key antioxidant factors (HO-1, UGT1A1, NQO1).Results: In vitro, HIPK2 inhibition markedly increased oxidative stress-induced cell death and significantly down-regulated UGT1A1 expression. In vivo, endogenous HIPK2 expression was significantly suppressed post-TBI. Conversely, HIPK2 overexpression effectively rescued the expression of antioxidant proteins UGT1A1 and NQO1. Conclusion: These results demonstrate that HIPK2 is a critical modulator of the antioxidant response after TBI, capable of orchestrating key defense genes and conferring neuroprotection. Our findings identify HIPK2 as a promising molecular target for therapeutic intervention against TBI-related oxidative damage.]]></abstract>
				<keyword_fa></keyword_fa>
				<keyword>Anti-oxidant response, HIPK2, Neuroprotection, Oxidative stress, Traumatic brain injury</keyword>
				<start_page>804</start_page>
				<end_page>811</end_page>
				<web_url>https://ijbms.mums.ac.ir/article_27554.html</web_url>
			<author_list><author>
				<first_name>Qiangbin</first_name>
				<middle_name></middle_name>
				<last_name>Zhu</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>zqbmail@yeah.net</email>
				<code>120983</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurosurgery, The Second Affiliated Hospital of Fujian Medical, Quanzhou, Fujian Province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Fan</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>wangfan_0426@sina.com</email>
				<code>120984</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurosurgery, The Second Affiliated Hospital of Fujian Medical, Quanzhou, Fujian Province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Bojun</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>horaisanrakui@fjmu.edu.cn</email>
				<code>120985</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurosurgery, The Second Affiliated Hospital of Fujian Medical, Quanzhou, Fujian Province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Zhigang</first_name>
				<middle_name></middle_name>
				<last_name>Pan</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>pzg582512@fjmu.edu.cn</email>
				<code>120986</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Neurosurgery, The Second Affiliated Hospital of Fujian Medical, Quanzhou , Fujian Province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Xiaodong</first_name>
				<middle_name></middle_name>
				<last_name>Kang</last_name>
				<suffix></suffix>
				<first_name_fa></first_name_fa>
				<middle_name_fa></middle_name_fa>
				<last_name_fa></last_name_fa>
				<suffix_fa></suffix_fa>
				<email>493828992@qq.com</email>
				<code>120987</code>
				<coreauthor>No</coreauthor>
				<affiliation>Department of Intensive Care Unit, The Second Affiliated Hospital of Fujian Medical, Quanzhou, Fujian Province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author><author>
				<first_name>Weipeng</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>hwpfjmu@yeah.net</email>
				<code>120988</code>
				<coreauthor>Yes</coreauthor>
				<affiliation>Department of Neurosurgery, The Second Affiliated Hospital of Fujian Medical, Quanzhou, Fujian Province, China</affiliation>
				<affiliation_fa></affiliation_fa>
				 </author></author_list>
				</article>
			</articleset>
			</journal>