International journal of molecular medicine最新文献

{"title":"Gomisin A as a multi‑target therapeutic agent: Pharmacological mechanisms, pharmacokinetics and network pharmacology (Review).","authors":"Jiaqi Xu, Sha Shi, Chengkai Zhu, Qi Sui, Shanhao Zhu, Jingnan Zhang, Yi Zhang, Peng Chen","doi":"10.3892/ijmm.2026.6011","DOIUrl":"https://doi.org/10.3892/ijmm.2026.6011","url":null,"abstract":"<p><p>Gomisin A (GA; C23H28O7) is a principal bioactive dibenzocyclooctadiene lignan derived from <i>Schisandra chinensis</i> (Turcz.) Baill. (Wu Wei Zi), a herb traditionally used in Chinese medicine for its adaptogenic, hepatoprotective and detoxifying properties, particularly in treating fatigue, chronic cough and liver disorders. GA exhibits multi‑target potential against a spectrum of complex diseases. The present study aimed to assess the pharmacological profile, mechanisms, pharmacokinetics (PK) and computational docking of GA, emphasizing its potential as a multi‑target agent. A comprehensive literature search was performed in the PubMed and China National Knowledge Infrastructure database platforms. All mechanistic findings were appraised and stratified by supporting evidence strength, complemented by network pharmacology screening, molecular docking and molecular dynamics (MD) assessment of representative target complexes. GA exhibits polypharmacological properties, including hepatoprotective, anticancer, cardiovascular‑modulating, neuroprotective and anti‑inflammatory/antioxidant effects, with hepatoprotection representing the most robustly supported preclinical indication. GA modulates key signaling pathways such as the PI3K/AKT/mTOR, MAPK and ErbB receptor family pathways. Network pharmacology analysis identified STAT3, EGFR and mTOR as high‑priority candidate targets. Molecular docking predicted moderate‑to‑strong binding affinity across nine hub proteins, with that of EGFR reaching ‑7.7 kcal/mol. MD simulations further supported the conformational plausibility of the GA‑EGFR, GA‑GSK3β and GA‑STAT3 complexes. PK data identified limited oral bioavailability as a key translational bottleneck. GA holds promise as a multi‑target natural product. Advancing GA toward clinical translation requires addressing PK limitations through advanced delivery systems, alongside orthogonal validation of its predicted targets and preclinical and clinical evaluation.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 6","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149193459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anesthetics and cancer biology: Translational evidence from perioperative modulation to drug repurposing (Review).","authors":"Ting Yang, Jiao Tang, Muhammad Saqib Mudabbar, Huan Hu, Qiang Fu, Chunlan Pu","doi":"10.3892/ijmm.2026.6007","DOIUrl":"https://doi.org/10.3892/ijmm.2026.6007","url":null,"abstract":"<p><p>Perioperative anesthesia is delivered during a brief but biologically dynamic interval in which surgical stress, inflammation, immune perturbation and tissue repair may alter the environment encountered by residual or disseminated tumor cells. Experimental studies indicate that anesthetic‑related agents can modify proliferation, apoptosis, epithelial‑mesenchymal transition, angiogenesis, immune surveillance and the tumor microenvironment. Translation to clinical benefit, however, has been inconsistent, in part because experimental models, routes and exposure schedules often differ substantially from perioperative pharmacology. Lidocaine and propofol illustrate this gap. In early breast cancer, a multicenter randomized trial reported improved 5‑year disease‑free and overall survival after preoperative peritumoral infiltration with 0.5% lidocaine, although independent confirmation is still required. By contrast, randomized comparisons of propofol‑based and volatile anesthesia, including long‑term follow‑up studies and GA‑CARES, have not demonstrated an overall‑ or disease‑free‑survival advantage for propofol. Mechanistic and perioperative biomarker studies remain informative, but these biomarkers are not validated surrogates for oncological outcomes. This review therefore evaluates anesthetic‑related interventions according to the exposure actually delivered, the level of mechanistic inference supported and the strength of clinical outcome evidence. Routine anesthetic choice should continue to follow established perioperative indications, whereas future cancer‑directed studies should align clinically achievable exposure with defined biological mechanisms, selected patient populations and clinically meaningful endpoints.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 6","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Expression of Concern] Multiple roles of SOCS proteins: Differential expression of SOCS1 and SOCS3 in atherosclerosis.","authors":"Xiao Liang, Ming He, Tao Chen, Yan Liu, Yu-Ling Tian, Yu-Liang Wu, Yan Zhao, Yan Shen, Zu-Yi Yuan","doi":"10.3892/ijmm.2026.6006","DOIUrl":"https://doi.org/10.3892/ijmm.2026.6006","url":null,"abstract":"<p><p>Following the publication of the above paper, it has been drawn to the Editor's attention by a concerned reader that, for the immunohistochemical images shown in Fig. 3 on p. 1070, the 'SOCS3/HD/16W' and 'SOCS3/CD/28W' images were apparently the same, albeit with differently coloured shading, suggesting that this figure had been assembled incorrectly. In addition, upon analyzing the data in this paper independently in the Editorial Office, it came to light that one of the histological images featured in Fig. 2A (the 'Oil Red O/12W' image) apparently reappeared in a paper written by different authors at different research institutes in the journal Redox Biology several years after the publication of this article, albeit the image in that paper did not feature the same level of clarity. The authors have been contacted by the Editorial Office to offer an explanation for the apparently incorrect assembly of the data in Fig. 3, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office conitnues to investigate this matter further. [International Journal of Molecular Medicine 31: 1066‑1074, 2013; DOI: 10.3892/ijmm.2013.1323].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 6","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149109271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi‑target mechanisms of paeoniflorin in inflammatory regulation: A network pharmacology (Review).","authors":"Jin Zhang, Junjie Ye, Kun Jin, Xuan Sun, Xinyu Yu, Yuan Zhao, Ni Zhu","doi":"10.3892/ijmm.2026.6010","DOIUrl":"10.3892/ijmm.2026.6010","url":null,"abstract":"<p><p>Paeoniflorin (PF), a monoterpene glycoside from Paeonia roots, shows low toxicity and broad anti‑inflammatory activity. A systematic review (PubMed, through 2025) with network pharmacology indicates that PF restores mitochondrial function, raises anti‑inflammatory mediators (IL‑10 and arginase‑1), reduces TNF‑α, IL‑1β and IL‑6, and eases oxidative stress. Its effects hinge on intertwined routes, dampening TLR4/MyD88, blocking NF‑κB nuclear entry, lowering MAPK phosphorylation, reshaping JAK‑STAT, and disrupting NLRP3 inflammasome assembly. Network mapping singles out a conserved core module (MAPK1, MAPK3, HSP90AA1, TP53, ESR1, BCL2, HIF1A, IL6, IL10 and FGF2), with HSP90AA1 and ESR1 as disease‑tailored effectors in rheumatoid arthritis and osteoarthritis (OA). PF absorbs fast and gathers in the liver with minimal toxicity, yet oral availability stays poor. Preclinical promise spans OA, colitis, and atherosclerosis, while clinical data remain thin. Synergistic pairing with other agents and structural refinement of PF broaden its reach, though such computational leads need experimental corroboration. Future efforts should improve its bioavailability, develop targeted delivery systems, and conduct rigorous clinical trials to move PF from tradition to evidence‑based medicine.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 6","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Expression of Concern] EETs and CYP2J2 inhibit TNF‑α‑induced apoptosis in pulmonary artery endothelial cells and TGF‑β1‑induced migration in pulmonary artery smooth muscle cells.","authors":"Wenjing Feng, Xizhen Xu, Gang Zhao, Geng Li, Tiantian Liu, Junjie Zhao, Ruolan Dong, Dao Wen Wang, Ling Tu","doi":"10.3892/ijmm.2026.6012","DOIUrl":"10.3892/ijmm.2026.6012","url":null,"abstract":"<p><p>Following the publication of the above paper, it has been drawn to the Editor's attention by a concerned reader that, for the cell migration assay experiments shown in Fig. 6A on p. 691, the 'Control' and 'TGF‑β1 + 14,15‑EET' data panels contained an overlapping section of data, such that these data, which were intended to show the results from differently performed experiments, appeared to have been derived from the same original source. The authors have been contacted by the Editorial Office to offer an explanation for the apparently incorrect assembly of data in Fig. 6, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office conitnues to investigate this matter further. [International Journal of Molecular Medicine 32: 685‑693, 2013; DOI: 10.3892/ijmm.2013.1435].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 6","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13673161/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149193430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Six3 promoting the migration and neural differentiation of BMSCs via Btg2‑mediated Akt signaling pathway activation: A therapeutic strategy for stroke.","authors":"Zhenqiang Fu, Zhixin Li, Limin Zhang, Wentao Hu, Hecheng Yang, Jingtao Wang","doi":"10.3892/ijmm.2026.6013","DOIUrl":"https://doi.org/10.3892/ijmm.2026.6013","url":null,"abstract":"<p><p>Bone marrow‑derived mesenchymal stem cell (BMSC) transplantation holds therapeutic potential for stroke; however, but its effectiveness requires optimization. The transcription factor Sine Oculis Homeobox Homolog 3 (Six3) regulates processes crucial for BMSC therapy, such as neural cell proliferation and differentiation. However, whether Six3‑modified BMSCs exert enhanced therapeutic effects on stroke remains unknown. In the present study, mouse BMSCs were isolated and identified using surface markers. Six3‑overexpressing BMSCs exhibited enhanced proliferative, migratory and neural differentiation capacities. RNA‑sequencing analysis comparing the gene expression profiles of BMSCs with and without Six3 overexpression identified BTG Anti‑Proliferation Factor 2 (Btg2) as an upregulated gene (log2FC=1.45, P<0.05) in Six3‑overexpressing cells. Further investigations revealed that Six3 directly binds to the TGATACTGTCT sequence within the Btg2 promoter and activates its transcription. Btg2 knockdown abolished the effects of Six3 overexpression. Mechanistically, Six3 promoted Akt phosphorylation via Btg2, enhancing BMSC viability and neural differentiation. A mouse model of stroke was established using transient middle cerebral artery occlusion (MCAO, 1.5‑h occlusion and 24‑h reperfusion). BMSCs were administered via tail vein injection at the onset of reperfusion. GFP expression detected in brain tissue at 24 h post‑reperfusion confirmed successful the homing of BMSCs to the brain. The transplantation of Six3‑overexpressing BMSCs ameliorated brain pathology, reducing apoptosis and cerebral infarct volume. Notably, Six3‑modified BMSCs demonstrated a significantly greater therapeutic efficacy than unmodified BMSCs. Collectively, these findings demonstrate that Six3 enhances the therapeutic properties of BMSCs by transcriptionally activating Btg2, which promotes Akt phosphorylation. These findings provide novel mechanistic insight into the optimization of stem cell therapy in stroke.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 6","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149192704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple strategies to improve the therapeutic efficacy of mesenchymal stem cell‑derived exosome transplantation in ischemic stroke (Review).","authors":"Yan Xu, Xiaolei Zhou, Wenhui Zeng, Jiabing Wang, Lin Zhou, Lincai Li, Zhengwei Zou, Cixiang Chen, Yichi Zhang, Zhengyi He, Junsong Ye","doi":"10.3892/ijmm.2026.6016","DOIUrl":"https://doi.org/10.3892/ijmm.2026.6016","url":null,"abstract":"<p><p>Ischemic stroke (IS) is a common cause of physical disability and death worldwide. Although it has been indicated that mesenchymal stem cells (MSCs) can treat IS through mechanisms such as immunomodulation, angiogenesis and neuroprotection, their clinical application is limited by inherent drawbacks, such as immune rejection risk and tumorigenic potential. Notably, MSC‑derived exosomes (MSC‑Exos) possess advantages, such as a smaller volume, low immunogenicity and low tumorigenicity, enabling therapeutic effects similar to those of the parent cells. Furthermore, MSC‑Exos can carry various bioactive substances and cross the blood‑brain barrier (BBB), thus indicating their potential in the diagnosis, treatment and prognostic assessment of IS. The present review comprehensively elaborates on the principles by which MSC‑Exos may treat IS through mechanisms such as inhibiting inflammatory responses, suppressing apoptosis, promoting angiogenesis, regulating ferroptosis and maintaining BBB integrity. However, the therapeutic efficacy of MSC‑Exo monotherapy is restricted by its low brain bioavailability, short lesion retention time, insufficient <i>in vivo</i> stability and inability to remain at the lesion site for an extended period of time to exert its effect. Furthermore, the review summarizes the recent optimization strategies involving the combination of MSC‑Exos with microRNAs, traditional Chinese medicine, hydrogels, exosome pretreatment and electroacupuncture to enhance the efficacy of MSC‑Exo therapy for IS, and systematically reviews their synergistic therapeutic mechanisms. In addition, the current status of clinical translation, technical breakthrough obstacles and future development directions for MSC‑Exo combination therapies in neurological diseases is outlined, providing a theoretical reference for innovative treatments of IS.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 6","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149193388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Expression of Concern] Gambogic acid inhibits invasion of osteosarcoma via upregulation of TIMP‑1.","authors":"Zeng-Feng Xin, Cheng-Chun Shen, Li-Jiang Tao, Shi-Gui Yan, Hao-Bo Wu","doi":"10.3892/ijmm.2026.6008","DOIUrl":"10.3892/ijmm.2026.6008","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the cell invasion assay data shown in Figs. 2A and 5A on p. 107 and p. 100 respectively, the '0 µM gambogic acid (GA)' data panel in Fig. 2A (upper left panel) contained overlapping sections of data with the 'SiRNA TIMP‑1' and the 'SiRNA + GA (1 µM)' data panels in Fig. 5A; furthermore, upon analyzing the data in this paper independently in the Editorial Office, it came to light that the '0 µM GA' and the '0.5 µM GA' data panels in Fig. 2A also contained an overlapping edge of data, suggesting that these data, which were intended to show the results from differently performed experiments, had apparently been derived from a smaller number of original sources. The authors have been contacted by the Editorial Office to offer an explanation for the apparently incorrect assembly of this pair of figures, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 31: 105‑112, 2013; DOI: 10.3892/ijmm.2012.1192].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 6","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of neuroimmune crosstalk in vestibular disorders: Linking inflammation with neural circuit dysfunction (Review).","authors":"Xianfang Pan, Jin Fan, Zhiyi Yang, Zegang Yin, Zhen Li, Zhifeng Rui, Hujun Zhang, Yujie Li, Hongjuan Zhang","doi":"10.3892/ijmm.2026.6009","DOIUrl":"https://doi.org/10.3892/ijmm.2026.6009","url":null,"abstract":"<p><p>Vestibular disorders such as vestibular migraine (VM) and Menière's disease (MD) involve complex interactions between inflammation and neural circuit dysfunction. Emerging evidence highlights neuroimmune crosstalk as a unifying pathophysiological framework. The present review synthesized current knowledge on inflammatory cytokine networks; neuropeptide signaling including calcitonin gene‑related peptide and histamine; glial responses; and systemic immune influences including the gut‑vestibular axis. Emerging evidence suggests potentially distinct immunological profiles may differentiate VM from MD. Illustrative examples include elevated IL‑1β and macrophage‑derived C‑X‑C motif chemokine ligand (CXCL)8 in MD, whereas CXCL10 acting through the PI3K/AKT signaling pathway has been implicated in VM pathogenesis. However, direct comparative studies remain limited and findings across cytokine studies show some heterogeneity. These observations support the concept of mechanism‑based subtyping as a promising framework requiring further validation. Neuroinflammation has dual effects on vestibular compensation, with appropriately calibrated responses promoting recovery and excessive or suppressed inflammation impairing plasticity. The present review integrates molecular, cellular and systemic neuroimmune mechanisms to provide a cohesive framework linking inflammation with vestibular neural circuit dysfunction. The purpose of the present study was to inform future biomarker development and precision therapeutic strategies for vestibular disorders.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 6","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol alleviates osteoarthritis progression by inhibiting NLRP3 inflammasome response via the AMPK/PPARγ signaling pathway.","authors":"Shanshan Cui, Zifan Luo, Wen Qin, Bo Chen, Qiaoxia Zhang, Jianbing Ma, Jie Ma, Rui Zhang","doi":"10.3892/ijmm.2026.6015","DOIUrl":"https://doi.org/10.3892/ijmm.2026.6015","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a chronic, degenerative disease affecting joint tissue. Resveratrol (RES), a natural polyphenolic compound, has anti‑inflammatory, antioxidant and anti‑apoptotic effects in chondrocytes and macrophages, suggesting therapeutic potential for OA. The present study investigated the molecular mechanisms of RES in OA treatment through network pharmacology analysis and <i>in vitro</i> and <i>in vivo</i> experiments. Network pharmacology was performed to identify potential therapeutic targets and pathways. An OA cell model was established by treating SW1353 cells with IL‑1β, followed by RES intervention without or with AMPK inhibitor to evaluate the effects on the AMPK/PPARγ signaling pathway, NLRP3 inflammasome response, and extracellular matrix (ECM) metabolism. For <i>in vivo</i> assays, OA mice were established through the destabilization of the medial meniscus (DMM) surgery, and administered RES through oral gavage. Histopathological changes, serum inflammatory factors and the expression of target proteins in articular cartilage were analyzed. Network pharmacology identified the AMPK/PPARγ pathway as a key mechanism underlying the therapeutic effects of RES in OA. <i>In vitro</i>, RES activated the AMPK/PPARγ pathway and inhibited the NLRP3 inflammasome response, thereby preserving ECM homeostasis in SW1353 cells. <i>In vivo</i>, RES alleviated OA progression by suppressing cartilage degeneration and synovitis, and regulating serum inflammatory levels. The target protein changes were consistent with the <i>in vitro</i> findings. The present study demonstrates that RES effectively regulates the NLRP3 inflammasome response by activating the AMPK/PPARγ signaling pathway, providing a valuable experimental foundation and potential clinical utility for RES as a complementary and alternative therapy for OA.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 6","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149192432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}