Iranian Journal of Basic Medical Sciences最新文献

{"title":"Comparison of long non-coding RNA NEAT1 expression, P53, and anti-oxidant factors between Alzheimer's patients and healthy individuals.","authors":"Sara Yarahmadi, Leila Alidoust, Alia Saberi, Behrooz Khakpour-Taleghani, Mohammad Rostampour, Adele Jafari","doi":"10.22038/ijbms.2026.89576.19336","DOIUrl":"10.22038/ijbms.2026.89576.19336","url":null,"abstract":"<p><strong>Objectives: </strong>Several studies have reported that the lncRNA Nuclear-enriched abundant transcript 1 (NEAT1) is associated with the progression of Alzheimer's disease (AD). Oxidative stress and apoptosis also play crucial roles in the development of AD. The present study compared the serum levels of NEAT1, superoxide dismutase (SOD), glutathione (GSH), and P53 between individuals with AD and healthy controls.</p><p><strong>Materials and methods: </strong>Peripheral blood samples were collected from 30 AD patients and 33 healthy controls and then centrifuged to separate serum. Total RNAs were isolated, and real-time polymerase chain reaction (RT-qPCR) was applied to determine NEAT1 gene expression. Also, Enzyme-linked immunoassays (ELISA) were conducted to measure SOD and GSH as anti-oxidant factors, and p53 as an apoptosis marker.</p><p><strong>Results: </strong>NEAT1 expression was significantly higher in AD patients than in controls (<i>P</i><0.001). In addition, ROC analysis revealed that serum NEAT1 levels distinguished AD patients from healthy controls with 90% sensitivity and 84.85% specificity. Moreover, the anti-oxidant levels of SOD (<i>P</i><0.0001) and GSH (<i>P</i><0.05) were significantly decreased in AD patients, while P53 levels were significantly increased (<i>P</i><0.05). However, no significant association was found between NEAT1 expression and the measured blood factors.</p><p><strong>Conclusion: </strong>The serum levels of NEAT1 effectively distinguished between AD patients and non-AD people, underscoring its potential as a blood-based biomarker for the development of Alzheimer's disease.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 4","pages":"598-604"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13213444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rosemary inhalation improves the behavior and cognition of vascular cognitive impairment rats by regulating SIRT1/mTOR pathway-mediated cell apoptosis and autophagy.","authors":"Fengfei Shi, Ensi Hong, Jiewei Bao, Wenguo Ye, Liping Wang, Hui Wang, Yanhui Zhang","doi":"10.22038/ijbms.2026.91451.19757","DOIUrl":"10.22038/ijbms.2026.91451.19757","url":null,"abstract":"<p><strong>Objectives: </strong>Vascular cognitive impairment (VCI) is a major cause of behavioral and cognitive abnormalities and dementia, but there are currently no specific drugs for VCI. Rosemary oil has been found to have a role in cognitive function. This study aims to evaluate whether inhalation of rosemary can improve learning and memory in VCI rats by regulating neuronal apoptosis and autophagy.</p><p><strong>Materials and methods: </strong>Male SD rats were used to establish a VCI rat model by bilateral common carotid artery ligation. The rats were intervened with rosemary essential oil inhalation and EX527 injection. Cognitive function was evaluated by the Morris water maze test two weeks after the operation. The pathological changes of hippocampal tissue (HE, Nissl, TEM, TUNEL) and protein expression (WB) were analyzed.</p><p><strong>Results: </strong>Compared with the sham group, the VCI group exhibited cognitive deficits, neuronal loss, mitochondrial damage, and increased neuronal apoptosis (<i>P</i><0.001). The levels of caspase-3, LC3B, and p-mTOR/mTOR in the hippocampal tissue were significantly elevated (<i>P</i><0.0001, <i>P</i><0.01, <i>P</i><0.01), while the protein level of SIRT1 was significantly reduced (<i>P</i><0.01). Compared with the VCI group, the rosemary group showed improved cognitive ability, ameliorated neuronal damage, and reduced neuronal apoptosis (<i>P</i><0.05). The levels of caspase-3, LC3B, and p-mTOR/mTOR were decreased (<i>P</i><0.0001, <i>P</i><0.01, <i>P</i><0.05), while the level of SIRT1 was increased (<i>P</i><0.05). However, intervention with EX527 attenuated this protective effect.</p><p><strong>Conclusion: </strong>Rosemary inhalation can improve behavior and cognition in VCI rats by regulating SIRT1/mTOR pathway-mediated cell apoptosis and autophagy.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 8","pages":"1269-1277"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioinformatic analysis and characterization of the anti-CD20 scFv-conjugated Fe₃O₄ nanoparticles for targeted therapy of CD20⁺ leukemia cells.","authors":"Shabnam Tavangarroosta, Mojgan Bandehpour, Masoumeh Rajabibazl, Farhood Najafi, Sepideh Ghani, Mahmoud Hassani, Bahram Kazemi","doi":"10.22038/ijbms.2026.95091.20508","DOIUrl":"10.22038/ijbms.2026.95091.20508","url":null,"abstract":"<p><strong>Objectives: </strong>Chronic lymphocytic leukemia (CLL) is one of the common types of leukemia. Various approaches for CLL therapy have been advanced, but they have some adverse effects. Iron oxide (Fe₃O₄) nanoparticles are promising drug carriers due to their magnetic properties and biocompatibility.</p><p><strong>Materials and methods: </strong>The recombinant anti-CD20 scFv was computationally modeled using the AlphaFold server. The complementarity-determining regions (CDR) of scFv were identified using the IMGT/V-Quest database. Molecular docking was performed separately between the scFv antibody and the CD20 antigen (ClusPro 2.0) and between Fe₃O₄ and the scFv (PyRx). Then, synthesized Fe₃O₄ nanoparticles were characterized using X-ray diffraction (XRD), field-emission scanning electron microscopy (FE-SEM), dynamic light scattering (DLS), and Fourier-transform infrared spectroscopy (FTIR). <i>In vitro</i> biological evaluation of the complexes was performed using the MTT assay.</p><p><strong>Results: </strong>The molecular docking studies revealed favorable interactions between the recombinant scFv antibody and the CD20 antigen. Fe₃O₄ nanoparticles were included as a simplified ligand model to explore possible surface interaction patterns with the scFv molecule, suggesting no predicted interactions with CDR regions in the docking model. Physicochemical characterization confirmed the successful synthesis and desirable structural attributes of the Fe₃O₄ nanoparticles. In vitro biological evaluation of the Fe₃O₄ nanoparticle--anti-CD20 scFv complex revealed that cell death in the Raji cell line was significantly higher than in the control groups, underscoring the targeted cytotoxic efficacy.</p><p><strong>Conclusion: </strong>These findings suggest that the Fe₃O₄ nanoparticle complex conjugated to an anti-CD20 scFv antibody can serve as a novel strategy for CLL treatment, contributing to the development of targeted therapies for cancer.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 8","pages":"1259-1268"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generation of oligodendrocyte precursor-like cells from mouse embryonic fibroblasts using miR-7a mimics.","authors":"Maryam Ghasemi-Kasman, Maryam Nakhaei-Nejad, Fatemeh Rabiei, Fabrizio Giuliani","doi":"10.22038/ijbms.2026.96127.20729","DOIUrl":"10.22038/ijbms.2026.96127.20729","url":null,"abstract":"<p><strong>Objectives: </strong>Developing effective strategies to enhance remyelination remains a major therapeutic challenge in demyelinating disorders such as multiple sclerosis (MS). MicroRNAs (miRNAs) have emerged as powerful regulators of cell fate. It has been shown that miR-7a is highly expressed in oligodendrocyte precursor cells (OPCs). This study aimed to investigate whether overexpression of miR-7a can reprogram mouse embryonic fibroblasts (MEFs) into OPC-like cells and oligodendrocytes <i>in vitro</i>.</p><p><strong>Materials and methods: </strong>MEFs were cultured, confirmed by vimentin immunostaining, and transfected with miR-7a mimics using Lipofectamine^TM 3000 or Lipofectamine^TM RNAiMAX reagent. Transfection efficiency was assessed by qRT-PCR analysis of miR-7a expression levels. Cells were then cultured in OPC induction medium and assessed for NG2 expression at 14 and 21 days post-transfection. Differentiation potential was examined by transferring induced cells into oligodendrocyte differentiation medium and analyzing O4 and MBP expression using Immunocytofluorescence.</p><p><strong>Results: </strong>Lipofectamine^TM RNAiMAX-mediated transfection produced significantly higher miR-7a expression than Lipofectamine^TM 3000, with a clear dose-dependent effect. MEFs transfected with miR-7a (10 and 20 pmol) exhibited NG2-positive cells at both 14 and 21 days, whereas no OPC markers were observed in negative controls or induction medium alone. Furthermore, miR-7a-induced OPC-like cells differentiated into O4⁺ and MBP⁺ oligodendrocytes, confirming their lineage potential.</p><p><strong>Conclusion: </strong>Overexpression of miR-7a successfully reprogrammed MEFs into OPC-like cells and promoted their differentiation into oligodendrocytes <i>in vitro</i>. These findings establish miR-7a as a potential tool for cell-based reprogramming strategies to generate OPC-like cells, warranting further investigation before translation into <i>in vivo</i> remyelination procedures for MS.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 10","pages":"1528-1534"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of key genes and pathways involved in trastuzumab resistance in HER2-positive gastric cancer through integrative bioinformatics analysis.","authors":"Feng Wang, Negar Mottaghi-Dastjerdi, Fatma Altameemi, Behzad Shahbazi, Nahid Ahmadi, Hamed Montazeri, Mohammad Soltany-Rezaee-Rad, Mohammad-Javad Niazi, Fateme Yazdani, Hamed Morad, Nana Li","doi":"10.22038/ijbms.2026.95195.20528","DOIUrl":"10.22038/ijbms.2026.95195.20528","url":null,"abstract":"<p><strong>Objectives: </strong>Trastuzumab resistance limits therapeutic efficacy in HER2-positive gastric cancer, and its systems-level regulatory architecture remains poorly characterized. This study aimed to identify key regulatory modules, biomarkers, and candidate therapeutic targets associated with trastuzumab resistance.</p><p><strong>Materials and methods: </strong>Gene expression profiles from trastuzumab-sensitive and -resistant gastric cancer cell lines (GSE77346) were analyzed to identify differentially expressed genes (DEGs). Protein-protein interaction (PPI) networks were constructed, and hub genes were identified using topology-based methods and clustering. Functional enrichment analysis was performed using Gene Ontology and KEGG pathways. Prognostic relevance was evaluated using TCGA-STAD data via UALCAN. Drug-gene interactions were explored using DrugBank and PHAROS, followed by structural modeling and molecular docking.</p><p><strong>Results: </strong>Trastuzumab resistance was linked to transcription factor-driven reprogramming, cytoskeletal and adhesion remodeling, and receptor tyrosine kinase (RTK) bypass signaling. Eleven hub genes were identified across four functional modules potentially associated with FGFR signaling, epithelial-mesenchymal transition (EMT), and lineage plasticity. Elevated PXDN and CDH2 expression was significantly associated with poor overall survival in TCGA-STAD. Molecular docking provided preliminary in silico evidence for potential interactions between selected compounds, including ADH-1, AGX51, artenimol, and phenethyl isothiocyanate, and candidate targets, including N-cadherin/CDH2, ID3, and vimentin.</p><p><strong>Conclusion: </strong>Trastuzumab resistance may involve networks related to transcriptional plasticity, adhesion dynamics, and RTK redundancy. This study provides a hypothesis-generating framework for future biomarker-guided combination strategies, which requires validation in HER2-positive cohorts and experimental models.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 10","pages":"1593-1604"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Radiosensitization effects of BaTiO₃ and gold nanoparticles in proton therapy of pancreatic tumors: A Monte Carlo study.","authors":"Elham Mansouri, Parinaz Mehnati","doi":"10.22038/ijbms.2026.95085.20513","DOIUrl":"10.22038/ijbms.2026.95085.20513","url":null,"abstract":"<p><strong>Objectives: </strong>This study investigates the potential of barium titanate (BaTiO₃) nanoparticles to enhance the therapeutic efficacy of proton therapy for pancreatic tumors in comparison to gold nanoparticles through both macroscopic and microscopic simulations.</p><p><strong>Materials and methods: </strong>Using the MCNP6.1 Monte Carlo code, we modeled a 3cm pancreatic tumor in the head of the pancreas loaded with clusters of BaTiO₃ and gold nanoparticles using a lattice model. Proton beam (SOBP, 135 MeV) interactions were simulated to evaluate the dose enhancement factor (DEF) within the tumor, the non-tumor pancreas, and Organs At Risks (OARs). Additionally, microscopic dosimetry was conducted to study the dose deposition in the vicinity of the clusters containing nanoparticles.</p><p><strong>Results: </strong>The gold nanoparticles present DEF of 1.21 and BaTiO₃ nanoparticles present DEF of 1.14 in the tumor site. The OARs remained mainly unaffected. Also, on a microscopic scale, DEF values of 1.7-1.83 in the presence of gold nanoparticles and 1.42-1.51 in the presence of BaTiO₃ nanoparticles were calculated. The microscopic DEFs were more than the macroscopic DEF.</p><p><strong>Conclusion: </strong>Both gold and BaTiO₃ nanoparticles enhanced proton dose deposition, with gold nanoparticles producing greater macroscopic and microscopic DEFs. The results also show that microscopic dose enhancement exceeds macroscopic dose enhancement, confirming that most proton-induced dose enhancement occurs in the close vicinity of nanoparticles. Because this study is based on Monte Carlo simulations with a uniform nanoparticle distribution and without biological modeling, further experimental studies are needed to validate these findings.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 10","pages":"1557-1563"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of autophagy and PI3K/Akt/mTOR pathway by naringin in sepsis-induced acute kidney injury.","authors":"Ali Tugrul Akin, Zeynep Yilmaz, Emin Kaymak, Şaban Varinli, Esra Onal, Necla Deger, Meryem Sayan, Derya Karabulut, Zuleyha Doganyigit, Ayse Toluk","doi":"10.22038/ijbms.2026.94607.20404","DOIUrl":"10.22038/ijbms.2026.94607.20404","url":null,"abstract":"<p><strong>Objectives: </strong>Sepsis-induced acute kidney injury (SI-AKI) is a life-threatening complication with limited treatment options, contributing to high morbidity and mortality worldwide. This study explores the renoprotective effects of naringin (NRG), a bioactive flavonoid, in a rat model of SI-AKI. It hypothesizes that NRG mitigates renal damage by enhancing autophagy and modulating the PI3K/Akt/mTOR pathway, thereby reducing oxidative stress, inflammation, and cellular injury.</p><p><strong>Materials and methods: </strong>Rats were divided into Control, NRG, LPS, LPS+NRG, and LPS+NRG+3-MA groups. NRG (100 mg/kg) was administered for 14 days, while LPS (10 mg/kg) induced sepsis. The LPS+NRG+3-MA group received 3-MA (30 mg/kg) to inhibit autophagy. Histopathological, immunohistochemical, gene expression, and biochemical analyses were performed. LPS-induced sepsis caused severe renal injury, including inflammation, tubular dilation, and oxidative stress (increased MDA, decreased catalase), alongside elevated TNF-α, NGAL, and KIM-1.</p><p><strong>Results: </strong>NRG treatment significantly preserved renal structure, reduced oxidative stress, and lowered TNF-α, NGAL, and KIM-1 levels. Immunohistochemistry showed increased Beclin-1 and LC3 expression in the LPS+NRG group, suggesting enhanced autophagy. Gene expression analysis revealed activation of the PI3K/Akt/mTOR pathway in NRG-treated rats.</p><p><strong>Conclusion: </strong>These findings indicate that NRG protects against SI-AKI by promoting autophagy and activating pro-survival pathways, offering a novel therapeutic strategy for sepsis management by regulating autophagy and modulating pathways.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 11","pages":"1677-1687"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effects of vitamin B12 against LPS-induced cognitive impairment through modulation of neuroinflammation, oxidative stress, and cholinergic dysfunction.","authors":"Zahra Khosravi, Rasul Saberi, Sajjad Mollaei, Elham Taheri, Afsaneh Hokmabadi, Zahra Kioumarsi Darbandi, Hassan Hazime, Arezoo Rajabian, Mahmoud Hosseini","doi":"10.22038/ijbms.2026.94516.20428","DOIUrl":"10.22038/ijbms.2026.94516.20428","url":null,"abstract":"<p><strong>Objectives: </strong>Neuroinflammation is a key pathological driver of cognitive impairment in neurodegenerative diseases. The endotoxin lipopolysaccharide (LPS) is used to model neuroinflammation, memory impairment, and neurodegeneration. Vitamin B12 has been extensively studied as an anti-oxidant and anti-inflammatory compound that plays an important role in neurological health. The protective effects of vitamin B12 against LPS-induced cognitive impairment, neuroinflammation, oxidative stress, and cholinergic dysfunction were investigated.</p><p><strong>Materials and methods: </strong>Male Wistar rats were randomly assigned to five groups (n=10 per group): Control, LPS (1 mg/kg, intraperitoneal injection), and three LPS+vitamin B12 (cyanocobalamin) groups receiving 0.25, 0.5, or 1 mg/kg of vitamin B12 by oral gavage. The Morris water maze and passive avoidance tests were conducted, and tissue samples were used to assess oxidative stress, inflammatory markers, and cholinergic activity in the animals' brains.</p><p><strong>Results: </strong>Vitamin B12 significantly improved memory in the Morris water maze and passive avoidance tests compared with the LPS group (<i>P</i><0.001), with higher doses being more effective. Vitamin B12 also attenuated oxidative stress and the mRNA expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 (<i>P</i><0.05-0.001). It also significantly decreased acetylcholinesterase activity (<i>P</i><0.01-0.001), while the highest dose significantly increased the expression of muscarinic acetylcholine receptor 1 (<i>P</i><0.01).</p><p><strong>Conclusion: </strong>These findings suggest that B12 may reduce inflammation and oxidative stress, modulate the cholinergic system, and have potential for the prevention and treatment of neuroinflammation and inflammation-induced memory impairment.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 11","pages":"1688-1698"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of the PKC-TRPV1-SP axis by propolis ameliorates chronic inflammatory pain in mice.","authors":"Jiayi Yu, Siyuan Yin, Hui Chen, Min Li, Juan Dong, Li Sun, Xueli Yin, Jing Wang","doi":"10.22038/ijbms.2026.89693.19378","DOIUrl":"10.22038/ijbms.2026.89693.19378","url":null,"abstract":"<p><strong>Objectives: </strong>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.</p><p><strong>Materials and methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 5","pages":"744-751"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13254776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148251546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Norepinephrine promotes the proliferation, migration, and phenotypic transformation of renal artery vascular smooth muscle cells via ROCK1.","authors":"Sixuan Chen, Lina Wang, Lu Wang, Hui Li, Junyao Lu, Yaxin He, Yihong Zhang, Yuanyuan Guo, Mingyu Liu","doi":"10.22038/ijbms.2026.90472.19527","DOIUrl":"10.22038/ijbms.2026.90472.19527","url":null,"abstract":"<p><strong>Objectives: </strong>This study investigated the role of norepinephrine (NE) and ROCK1 in regulating renal artery vascular smooth muscle cells (rVSMCs).</p><p><strong>Materials and methods: </strong>rVSMCs were treated with NE, and ROCK1 expression was assessed. Cell proliferation, migration, and phenotypic switching were evaluated using EdU incorporation and wound-healing assays. ROCK1 was silenced by siRNA. Mitochondrial membrane potential and morphology were analyzed to determine NE-induced mitochondrial alterations.</p><p><strong>Results: </strong>NE significantly up-regulated ROCK1 expression in rVSMCs. It promoted proliferation, migration, and phenotypic switching, as indicated by increased expression of proliferative and migratory markers, whereas ROCK1 silencing attenuated these effects. NE also reduced mitochondrial membrane potential and induced mitochondrial fission, suggesting an additional mechanism contributing to vascular remodeling.</p><p><strong>Conclusion: </strong>NE promotes rVSMCs proliferation, migration, and phenotypic switching through ROCK1 activation and alters mitochondrial dynamics. These findings identify the NE-ROCK1 axis as a critical mediator of vascular remodeling in hypertensive nephropathy and suggest it may serve as a promising therapeutic target.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 4","pages":"605-612"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13213450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}