Iranian Journal of Basic Medical Sciences最新文献

{"title":"An <i>in vivo</i> study on sonodynamic effects mediated by nanomicelles containing PpIX as a sonosensitizing agent.","authors":"Maryam Bakhshizadeh, Mehdi Hoseini, Samaneh Soudmand Salarabadi, Naser Tayebi-Meybodi, Ameneh Sazgarnia, Bahareh Khalili Najafabad","doi":"10.22038/ijbms.2025.90437.19489","DOIUrl":"10.22038/ijbms.2025.90437.19489","url":null,"abstract":"<p><strong>Objectives: </strong>Sonodynamic therapy (SDT) is a promising non-invasive adjuvant approach for treating accessible tumors, requiring ultrasound (US) waves, sonosensitizing molecules, and oxygen. However, sonosensitizers such as protoporphyrin IX (PpIX) face limitations, including poor water solubility, phototoxicity, and lack of targeting. To address these issues, we encapsulated PpIX in biocompatible nanomicelles to enhance solubility, reduce side effects, and improve tumor targeting.</p><p><strong>Materials and methods: </strong>After synthesizing, characterizing, and assessing the cytotoxicity of PpIX-loaded nanomicelles, the optimal concentration was selected. The 4T1 cell line was used to create a breast tumor model in BALB/c mice. To investigate the effect of SDT mediated by PpIX-loaded nanomicelles, tumors were exposed to US at 800 and 2400 kHz simultaneously, 10 min after intratumoral injection of the drug. The tumors were measured with a digital calliper, and tumor volume was calculated at specific time intervals and compared. The tumor tissue necrosis percentage was determined by pathological examination, and the volume loss in different groups was quantified.</p><p><strong>Results: </strong>SDT with PpIX nanomicelles significantly reduced tumor volume within 7 days compared with controls (<i>P</i><0.05), with the greatest volume loss observed in this group. Pathological analysis confirmed extensive tumor necrosis.</p><p><strong>Conclusion: </strong>PpIX-loaded nanomicelles enhance SDT efficacy in breast tumors, demonstrating potential as a targeted delivery system. Repeated treatments may further inhibit tumor growth.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 2","pages":"225-230"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722848","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":"Investigating the protective effect of zinc supplementation on streptozotocin-induced pancreatic beta-cell damage via the HMGB1/TLR2/MAPK pathway.","authors":"Sahin Yesildag, Elvan Yılmaz Akyüz, Eylem Taskin","doi":"10.22038/ijbms.2026.92275.19914","DOIUrl":"10.22038/ijbms.2026.92275.19914","url":null,"abstract":"<p><strong>Objectives: </strong>This study investigated the protective effect of zinc supplementation on insulin release via modulation of the High Mobility Group Box 1 (HMGB1)/Toll-like receptor 2 (TLR2)/mitogen-activated protein kinase (MAPK) signaling pathway in streptozotocin (STZ)-induced pancreatic β-cell injury, a commonly used model of type 1 diabetes.</p><p><strong>Materials and methods: </strong>Human pancreatic β-cells (1.1B4) were divided into five groups: Control, Diabetes, Diabetes + Zinc, Diabetes + Box A, and Diabetes + Zinc + Box A. Diabetes was induced with STZ (20 mM, four hours, type-1), followed by treatment with zinc (30 μM) and/or Box A (100 ng/l). Cellular oxidative stress, apoptosis, mitochondrial membrane potential (MMP), cell viability, and insulin secretion were measured. Protein expressions of HMGB1, TLR2/4, extracellular signal-regulated kinases 1/2 (ERK1/2), and c-Jun N-terminal kinase (JNK) were analyzed using western blotting.</p><p><strong>Results: </strong>Zinc supplementation restored MMP and total antioxidant status (TAS), reduced apoptotic cell death, and enhanced TLR2 and ERK1/2 expression suppressed by STZ. Combined zinc and Box A treatment markedly increased insulin secretion under both hypo- and hyperglycemic conditions.</p><p><strong>Conclusion: </strong>Zinc exerts protective effects against STZ-induced β-cell damage, likely through modulation of the HMGB1/TLR2/MAPK axis. These findings highlight the therapeutic potential of zinc supplementation in protecting pancreatic β-cell function in diabetes mellitus.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 7","pages":"1020-1026"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874100","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":"Combined cold atmospheric plasma and vemurafenib suppress MITF-P21 signaling and MMP-driven metastasis in cutaneous melanoma.","authors":"Zahra Yazdani, Mansooreh Mirzaei, Sadegh Fattahi, Farshad Sohbatzadeh, Saeid Abediankenari, Arefe Mousavi, Fatemeh Mirbabaei, Zeinab Rostami, Monireh Golpour, Alireza Rafiei","doi":"10.22038/ijbms.2026.95374.20566","DOIUrl":"10.22038/ijbms.2026.95374.20566","url":null,"abstract":"<p><strong>Objectives: </strong>This study investigated the anti-tumor efficacy of combined cold atmospheric plasma (CAP) and Vemurafenib (VEM) treatment (CAP plus VEM) in cutaneous melanoma, focusing on the MITF-P21 axis and MMP-driven metastasis.</p><p><strong>Materials and methods: </strong>The therapeutic effects of CAP and VEM were evaluated using <i>in vitro</i> and <i>in vivo</i> models. B16-F10 melanoma and L929 fibroblast cell lines were used to assess long-term cell proliferation and migration using clonogenic and wound-healing assays. <i>In vivo</i>, melanoma tumors were induced in C57BL/6 mice, followed by treatment with CAP, VEM, or CAP plus VEM. Tumor tissues and major organs were collected for histopathological evaluation and molecular analysis. Gene expression levels of MITF, P21, MMP-2, and MMP-9 were quantified by qRT-PCR in both experimental settings.</p><p><strong>Results: </strong>CAP and VEM significantly inhibited melanoma cell proliferation and migration, with the CAP plus VEM showing the most pronounced effect. In vitro, all treatments markedly down-regulated <i>MITF</i>, <i>P21</i>, and <i>MMP-2</i> gene expression (<i>P</i><0.0001). Histopathological analysis revealed extensive tumor necrosis, reduced cellularity, and improved tissue architecture in the CAP plus VEM group, accompanied by fewer metastatic alterations in major organs. qRT-PCR of tumor tissues confirmed significant down-regulation of <i>MMP-2</i> and <i>MMP-9</i> after CAP, VEM, and especially the CAP plus VEM group (<i>P</i><0.0001). The modest <i>in vivo</i> changes in <i>MITF</i> and <i>P21</i> may reflect microenvironmental influences.</p><p><strong>Conclusion: </strong>The CAP plus VEM enhances anti-tumor efficacy and suppresses metastasis-related pathways in melanoma, both <i>in vitro</i> and <i>in vivo</i>. This suggests a promising complementary therapeutic strategy.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 10","pages":"1564-1574"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038616","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":"Imperatorin alleviates post-infarction cardiac fibrosis via the CD44/PI3K/AKT pathway in mice.","authors":"Hui Yuan, YanKun Hao, Mohammed Alaa Abdulzahra, YueYing Yuan, Xuan Li, Javeria Qadir, ManYu Wang, YuanYuan Zhang, TingTing Li, Jian Sun","doi":"10.22038/ijbms.2026.95833.20660","DOIUrl":"10.22038/ijbms.2026.95833.20660","url":null,"abstract":"<p><strong>Objectives: </strong>This study examines the effects of imperatorin (IMP) on cardiac fibrosis in mice with myocardial infarction (MI) and seeks to elucidate the underlying molecular mechanisms.</p><p><strong>Materials and methods: </strong>C57BL/6 mice were randomly assigned to a control group, an ISO-induced MI group, and ISO+IMP treatment groups (7.5, 15, and 30 mg/kg). 4D-FastDIA-based quantitative proteomics was used for global proteomic analysis to identify differentially expressed proteins (DEPs) and signaling pathways involved in the anti-fibrotic effects of IMP following MI. Echocardiography was performed to evaluate cardiac function; histopathological analysis and serological indicators were used to assess myocardial injury; and Western blotting was employed to verify the expression and mechanisms of related proteins.</p><p><strong>Results: </strong>Compared with the ISO group, IMP treatment markedly improved electrocardiographic abnormalities, reduced serum LDH and cTn-I levels, enhanced cardiac function, and attenuated myocardial injury and fibrosis. Proteomic analysis identified 98 DEPs in the ISO/Control group and 127 DEPs in the ISO+IMP/ISO group. GO and KEGG analyses showed that these DEPs were mainly enriched in fibroblast proliferation-related biological processes and ECM-receptor interaction pathways, with significant involvement of the PI3K/AKT signaling pathway. PPI network analysis highlighted FN1, VTN, Colα2(I), Colα1(III), and CD44 as key regulatory proteins, among which CD44 was notably down-regulated by IMP. Molecular docking demonstrated strong binding affinity between IMP and CD44. Western blot results further confirmed that IMP significantly reduced the expression of fibrosis-related proteins and suppressed activation of the CD44/PI3K/AKT signaling pathway.</p><p><strong>Conclusion: </strong>IMP ameliorates myocardial fibrosis in MI mice by modulating the CD44/PI3K/AKT signaling pathway.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 11","pages":"1659-1669"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669784/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216077","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":"Sappanone A suppresses CHOP expression and exerts neuroprotective effects in epilepsy.","authors":"Jie Fu, Jinglun Li, Xiu Chen","doi":"10.22038/ijbms.2026.95426.20696","DOIUrl":"10.22038/ijbms.2026.95426.20696","url":null,"abstract":"<p><strong>Objectives: </strong>Sappanone A (SA) is a compound derived from <i>Caesalpinia sappan</i> L that exhibits multiple biological effects, including anti-apoptotic, anti-inflammatory, and anti-oxidant activities. Because oxidative stress, cell apoptosis, and neuroinflammation are associated with the pathophysiology of epilepsy, we conducted this study to explore the role of SA in epilepsy.</p><p><strong>Materials and methods: </strong>We used SA to treat pentylenetetrazole (PTZ)-induced mice as well as HT22 hippocampal cells exposed to Mg²⁺-free solution. Seizure behavior in the mice was recorded. Nissl staining, TUNEL assay, and flow cytometry were used to evaluate neuronal damage and apoptosis. Moreover, we employed biochemical tests to assess inflammation and oxidative stress levels, and conducted quantitative reverse transcription polymerase chain reaction and western blot to detect CHOP expression.</p><p><strong>Results: </strong>Pretreatments with SA (25 and 50 mg/kg) significantly prolonged seizure latency and reduced seizure duration in PTZ-induced epileptic mice (all <i>P<</i>0.001), whereas 10 mg/kg had no significant effects. At effective doses, SA also alleviated neuronal damage, reduced inflammation, and attenuated oxidative stress (all <i>P<</i>0.05). Furthermore, SA suppressed CHOP expression, and CHOP overexpression partially reversed SA's protective effects (<i>P<</i>0.05).</p><p><strong>Conclusion: </strong>Our findings suggest that SA pretreatment exerts neuroprotective effects against epilepsy, potentially through suppression of CHOP expression. However, the causal relationship between CHOP suppression and SA-mediated neuroprotection in epilepsy warrants further investigation.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 11","pages":"1699-1707"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216311","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":"18β-Glycyrrhetinic acid-loaded silver nanoparticles mitigate neuroinflammation and endoplasmic reticulum stress in the brain tissue of diabetic rats.","authors":"Seçil Nazife Parlak, Seda Yakut, Adem Kara, Özlem Demi̇r, Saime Özbek Şebi̇n","doi":"10.22038/ijbms.2025.86986.18801","DOIUrl":"10.22038/ijbms.2025.86986.18801","url":null,"abstract":"<p><strong>Objectives: </strong>Diabetes mellitus (DM) causes oxidative stress, neuroinflammation, and endoplasmic reticulum (ER) dysfunction that contribute to neurodegeneration. This study investigated the effects of 18β-glycyrrhetinic acid-loaded silver nanoparticles (18β-GA-AgNPs) on brain injury in diabetic rats.</p><p><strong>Materials and methods: </strong>Fifty-six male Wistar rats were divided into eight groups: Sham, 18β-GA, AgNPs, 18β-GA-AgNPs, DM, DM+18β-GA, DM+AgNPs, and DM+18β-GA-AgNPs. Diabetes was induced by alloxan (120 mg/kg, IP), and treatments were administered orally for 14 days. Biochemical markers (MDA, GSH, SOD), histopathology, and expression of ER stress and apoptotic proteins (ATF6, IRE1, Caspase-3, BCL-2, CREB, TNF-α, and IL-1β) were evaluated.</p><p><strong>Results: </strong>The DM group exhibited significant increases in MDA, TNF-α, IL-1β, ATF6, and Caspase-3 with reduced GSH, SOD, and BCL-2, indicating oxidative stress, inflammation, apoptosis, and ER stress. In contrast, IRE1 levels remained unchanged in DM rats but showed a slight elevation in the AgNPs group. Treatment with 18β-GA-AgNPs markedly reduced MDA, TNF-α, IL-1β, ATF6, and Caspase-3, while restoring GSH, SOD, BCL-2, and CREB expression. Histopathological analysis confirmed neuronal apoptosis and perivascular and extracellular space enlargement in DM rats, whereas 18β-GA-AgNPs substantially attenuated these changes. Overall, 18β-GA-AgNPs provided synergistic neuroprotection by suppressing oxidative stress, inflammation, and ER stress while enhancing antioxidant and anti-apoptotic defenses.</p><p><strong>Conclusion: </strong>These findings suggest that 18β-GA-AgNPs may represent a promising therapeutic strategy against diabetes-associated neurodegeneration, although further long-term, ultrastructural, and sex-inclusive studies are warranted.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 1","pages":"81-89"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118873","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":"Comparative effects of estradiol and daidzein on the expression of endometrial cancer-related genes and histopathological parameters in the uterus of ovariectomized rats.","authors":"Vahid Setayesh, Asma Neisy, Maryam Niknam, Zahra Khoshdel, Farhad Koohpeyma, Sanaz Alaee, Fatemeh Zal","doi":"10.22038/ijbms.2025.89681.19349","DOIUrl":"10.22038/ijbms.2025.89681.19349","url":null,"abstract":"<p><strong>Objectives: </strong>This study compared the effects of daidzein (DZD) and 17-β-estradiol (E2) on uterine histopathology, expression of endometrial cancer-related genes, and anti-oxidant status in ovariectomized (OVX) rats.</p><p><strong>Materials and methods: </strong>Thirty rats were divided into five groups (n=6): Sham, OVX, OVX+E2 (10 μg/kg/day), OVX+DZD (20 mg/kg/day), and DZD-only. After 50 days of treatment, uterine tissues were analyzed for histopathological changes, mRNA expression of ERα, ERβ, PTEN, EZH2, and Ki67, and oxidative stress markers (TAC, SOD, CAT, and MDA).</p><p><strong>Results: </strong>Ovariectomy induced endometrial atrophy, significantly downregulated the expression of all target genes (ERα, ERβ, PTEN, EZH2, and Ki67), decreased SOD and CAT activity and TAC level, and increased MDA. E2 treatment reversed these changes but induced hyperplastic effects. DZD administration significantly increased CAT and SOD activity and elevated ERβ and Ki67 expression compared with the OVX group. Crucially, DZD prevented uterine atrophy without inducing hyperplasia.</p><p><strong>Conclusion: </strong>DZD demonstrated a potentially beneficial effect by improving uterine anti-oxidant capacity and preventing atrophy, but without the hyperplastic changes associated with estradiol. These findings suggest that DZD may be a safer alternative for managing hypoestrogenic conditions, warranting further investigation.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 1","pages":"145-154"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118901","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":"Electroacupuncture improves hypoxic stress and energy metabolism to alleviate vascular cognitive impairment through activation of the HIF-1α/p53/NGB signaling pathway in rats.","authors":"Peijia Hu, Fangyuan Xu, Wendong Zhang, Lin Bai, Fan Dai, Yu Ye, Jingji Wang, Hongliang Cheng","doi":"10.22038/ijbms.2025.86988.18796","DOIUrl":"10.22038/ijbms.2025.86988.18796","url":null,"abstract":"<p><strong>Objectives: </strong>We aimed to demonstrate that electroacupuncture (EA) alleviates vascular cognitive impairment (VCI) induced by cerebral ischemia in rats by modulating oxygen homeostasis and energy metabolism through the HIF-1α/p53/NGB signaling pathway.</p><p><strong>Materials and methods: </strong>Male Sprague‒Dawley rats underwent bilateral common carotid artery occlusion (BCCAO) to establish a VCI model. EA was administered once daily for 30 min over two weeks. Thirty minutes prior to EA, the hypoxia-inducible factor-1α (HIF-1α) inhibitor 2-methoxyestradiol (2ME2) was injected intraperitoneally. Cognitive function following BCCAO and EA was assessed using the Morris water maze test. Western blotting was performed to analyze the protein expression of HIF-1α, heme oxygenase-1 (HO-1), and neuroglobin (NGB). In addition, p53 mRNA expression was quantified by real-time PCR, and energy metabolite levels were determined using ELISA.</p><p><strong>Results: </strong>EA significantly improved learning and memory in VCI model rats. Histopathological analysis revealed that EA attenuated neuronal apoptosis and ultrastructural damage in the cortex and hippocampus. EA upregulated HIF-1α, NGB, and HO-1 expression but downregulated p53 mRNA expression in these regions. Moreover, EA treatment reversed the expression of glucose, lactic acid, and acetone aldehyde. Notably, the beneficial effects of EA on cerebral energy metabolism were abolished by 2ME2 in VCI model rats.</p><p><strong>Conclusion: </strong>EA alleviated BCCAO-induced neurological impairment and cognitive dysfunction in rats, possibly by reducing hypoxic stress and enhancing energy metabolism in the cortex and hippocampus, potentially through modulation of the HIF-1α/p53/NGB signaling pathway.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 1","pages":"34-42"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118994","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":"Raspberry protective role in inflammatory diseases: An overview.","authors":"Priyanka Arya, Vikram Sharma, Priyanka Singh, Rahul Sagar, Surabhi Thapliyal, Manu Sharma","doi":"10.22038/ijbms.2025.89042.19218","DOIUrl":"10.22038/ijbms.2025.89042.19218","url":null,"abstract":"<p><p>Inflammation is a natural immune response triggered by multiple factors such as pathogens, damaged cells, and toxic substances. These triggers can lead to both acute and chronic inflammatory reactions in different tissues, contributing to the development of several inflammatory disorders, including cardiovascular diseases, neuroinflammation, arthritis, and cancer. Both infectious and non-infectious stimuli activate immune cells and initiate critical inflammatory signaling pathways. Raspberries (<i>Rubus idaeus</i>) are abundant in bioactive constituents, especially polyphenols like anthocyanins, flavanols, phenolic acids, urolithin A, and ellagic acid, all of which possess notable anti-inflammatory and anti-oxidant activities. These compounds have been shown to regulate various inflammatory signaling pathways, including MAPKs, NF-κB, PI3K/Akt, AP-1, IL-6, TNF-α, IL-1β, CD40, nitric oxide (NO), caspases, and the JAK-STAT pathway. Studies have emphasized their broad pharmacological effects, such as anti-inflammatory, anti-oxidant, hepatoprotective, cardioprotective, gastroprotective, anti-obesity, skin depigmenting, and bone-regenerative properties. This review emphasizes mechanistic insights into raspberries' protective roles in managing inflammatory-related disorders, particularly cardiovascular diseases, neurodegenerative conditions, and cancer, and highlights their therapeutic potential.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 1","pages":"22-33"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146119016","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":"Kurarinone: From chemistry to pharmacological values-A review.","authors":"Huy Dinh Vu, Huynh Thi Ngoc Ni, Tran Thi Thanh Thuy, Ninh The Son","doi":"10.22038/ijbms.2026.92633.19997","DOIUrl":"10.22038/ijbms.2026.92633.19997","url":null,"abstract":"<p><p>Kurarinone (KRN) is a major prenylated flavanone isolated from <i>Sophora flavescens</i>, 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,\" \"<i>Sophora flavescens</i> flavonoids,\" \"prenylated flavanones,\" and related terms. Studies reporting natural occurrence, chemical isolation, biotransformation, physicochemical properties, pharmacological mechanisms, pharmacokinetics, and toxicity were included. <i>In vitro</i> and <i>in vivo</i> 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.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"29 5","pages":"675-687"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13254808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148251538","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}