Molecular immunology最新文献

{"title":"The dysregulation of B cells in systemic lupus erythematosus","authors":"Xinfeng Wu ,&nbsp;Xin Ma ,&nbsp;Bei Zhang ,&nbsp;Na Kang ,&nbsp;Yian E. Liu ,&nbsp;Xiaofei Shi ,&nbsp;Wanli Liu","doi":"10.1016/j.molimm.2026.01.009","DOIUrl":"10.1016/j.molimm.2026.01.009","url":null,"abstract":"<div><div>B cells are pivotal components of the immune system, responsible for antibody production and immune regulation. Aberrant B cell activation is central to the pathogenesis of systemic lupus erythematosus (SLE), driven by dysregulations of multiply signaling pathways, including B cell receptor (BCR), Toll-like receptor (TLR7/9), B cell-activating factor receptor (BAFF-R), and B-T cell interactions, along with related cytokines and interferons. These aberrant signaling pathways play diverse and integrated roles in SLE progression, contributing to autoantibody generation and tissue damage. This review examines the mechanisms linking aberrant B cell activation to SLE development, highlights recent genetic, epigenetic, and clinical insights, and discusses their implications for therapeutic management. Collectively, it provides a useful resource for researchers and clinicians in immunology and autoimmunity, enhancing the comprehension of B cell dysregulation in SLE.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"190 ","pages":"Pages 152-161"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078759","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":"HSPH1 and DNAJB1 as potential key regulators in hepatic ischemia-reperfusion injury","authors":"Shaomei Wu ,&nbsp;Wei Zhou ,&nbsp;Hong Duo ,&nbsp;Jian You,&nbsp;Yuanyuan Chen,&nbsp;Siqi Du,&nbsp;Ningbo Ku,&nbsp;Jun Luo,&nbsp;Zhongzhong Liu,&nbsp;Qifa Ye","doi":"10.1016/j.molimm.2026.01.001","DOIUrl":"10.1016/j.molimm.2026.01.001","url":null,"abstract":"&lt;div&gt;&lt;div&gt;Hepatic ischemia-reperfusion injury (HIRI) is a common and inevitable pathological event during liver transplantation and hepatectomy, which significantly impairs postoperative liver function recovery and patient prognosis. However, the molecular and cellular mechanisms of HIRI have not been fully elucidated and further research is urgently needed. In recent years, the rapid development of bioinformatics analysis technology and the research method combining multi-dimensional data mining with experimental verification have become important strategies for exploring the mechanisms of complex diseases. Building on this, this study aims to screen and analyze the potential roles and mechanisms of key regulatory factors in the process of HIRI through systematic bioinformatics analysis and experimental verification, providing a basis for clarifying its pathogenesis and finding potential therapeutic targets. In this study, two transcriptome microarray datasets (GSE14951 and GSE7706) of human liver tissue were systematically analyzed, and candidate genes related to IRI were initially screened through differential expression analysis. Combined with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, protein–protein interaction (PPI) network construction and modular analysis were performed to identify potential key regulatory factors, ultimately highlighting HSPH1 and DNAJB1. Subsequently, based on a mouse liver IRI model, paired reperfusion tissue samples from clinical liver transplant patients, and an AML12 cell hypoxia/reoxygenation (H/R) model, the two genes were experimentally validated from multiple perspectives, including transcriptional expression, protein levels, and subcellular localization. A combination of quantitative PCR (qPCR), Western blotting, immunohistochemistry (IHC), immunofluorescence (IF), and co-immunoprecipitation (Co-IP) was employed to comprehensively evaluate their expression dynamics, subcellular distribution, and protein–protein interaction characteristics. Differential expression analysis identified 154 genes with consistent expression trends across the two datasets, which were significantly enriched in metabolic, stress response, inflammatory, and protein folding pathways. PPI network construction and module analysis further identified HSPH1 and DNAJB1 as core components of a heat shock protein interaction cluster. Validation using a mouse IRI model, paired reperfusion tissue samples from clinical liver transplant patients, and an AML12 cell hypoxia/reoxygenation (H/R) model demonstrated that both genes were significantly upregulated under IRI conditions, localized in the cytosol, and exhibited co-localization and physical interaction. Transcription factor prediction analysis suggested that STAT3 and NR1I2 might be involved in their transcriptional regulation.&lt;/div&gt;&lt;div&gt;In conclusion, HSPH1 and DNAJB1 are co-expressed and physically interact in hepatic IRI, suggesting th","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"190 ","pages":"Pages 56-71"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978734","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":"Toddalia asiatica (L.) Lam. induces apoptosis in rheumatoid arthritis fibroblast-like synoviocytes by modulating the PI3K/AKT/NF-κB pathway","authors":"Jianjun Niu ,&nbsp;Chaocao Yan ,&nbsp;Fanyong Zeng ,&nbsp;Huanzhen Wang ,&nbsp;Zhiliang Fan ,&nbsp;Yihui Chai ,&nbsp;Chunyan Liu","doi":"10.1016/j.molimm.2026.01.008","DOIUrl":"10.1016/j.molimm.2026.01.008","url":null,"abstract":"<div><h3>Background</h3><div>Rheumatoid arthritis (RA) is an autoimmune disease. Although current pharmacological treatments can alleviate symptoms, they are often associated with significant adverse reactions and fail to halt disease progression. Therefore, there is an urgent need to develop novel therapies derived from natural resources that have broad immunomodulatory effects with minimal side effects. The root of <em>Toddalia asiatica</em> (L.) Lam. (TA), a traditional remedy used by the Tujia and Miao ethnic groups for rheumatism, represents a promising natural candidate for RA treatment. However, its specific mechanism of action in RA is not fully elucidated.</div></div><div><h3>Methods</h3><div>Collagen-induced arthritis (CIA) rat models and interleukin-1β (IL-1β)-stimulated fibroblast-like synoviocyte (FLS) models were established to assess the therapeutic effects of TA on RA. Network pharmacology analysis was performed to identify potential therapeutic targets and associated pathways. Cellular functions were assessed through CCK-8, wound healing, and transwell migration assays. Apoptosis was evaluated using TUNEL staining and flow cytometry analysis. mRNA and protein expression levels were determined by qPCR, Western blotting, immunofluorescence, and immunohistochemical staining.</div></div><div><h3>Results</h3><div>TA alleviated joint swelling in CIA rats by reducing serum levels of pro-inflammatory cytokines and reactive oxygen species (ROS). It also modulated the Bax/Bcl-2 ratio and induced synovial cell apoptosis. Network pharmacology analysis revealed that common targets between TA and RA were enriched in the PI3K/AKT/NF-κB pathway. In vitro studies showed that TA inhibited the proliferation, migration, and invasion of MH7A cells, decreased the secretion of pro-inflammatory cytokines and ROS production, and promoted apoptosis. Mechanistically, TA suppressed the phosphorylation of key proteins in the PI3K-AKT and NF-κB pathways and reduced the nuclear translocation of NF-κB.</div></div><div><h3>Conclusions</h3><div>TA exerts anti-RA effects by inhibiting the PI3K/AKT/NF-κB pathways and modulating the apoptosis balance of synovial fibroblasts. These findings provide a theoretical foundation for the clinical application of TA in RA treatment.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"190 ","pages":"Pages 125-139"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078160","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":"The activation of glial cells is involved in the pain and pruritus in allergic contact dermatitis","authors":"Wenzhang Dai ,&nbsp;Zhenglang Zhang ,&nbsp;Tengyun Xu,&nbsp;Kexin Cai,&nbsp;Anqi Luo,&nbsp;Zhenhui Luo,&nbsp;Ranjing Wang,&nbsp;Ziwei Lai,&nbsp;Junlin Wang,&nbsp;Hong Nie","doi":"10.1016/j.molimm.2026.01.007","DOIUrl":"10.1016/j.molimm.2026.01.007","url":null,"abstract":"<div><h3>Background</h3><div>The activation of glial cells in the central nervous system plays an important role in the neural signaling of chronic pain and pruritus. However, their involvement in the neural signaling of chronic pain and pruritus in ACD remains to be investigated. To determine the effect of spinal glial cell activation in the coexistence of chronic pain and pruritus in the ACD model, we observed spinal glial cell activation in a mouse model of ACD induced by SADBE.</div></div><div><h3>Methods</h3><div>Square acid dibutyl ester (SADBE) was employed to establish ACD model mice and monitor the activation of spinal cord glial cells. Additionally, the Gene Expression Omnibus (GEO) database was utilized to analyze potential mechanisms.</div></div><div><h3>Results</h3><div>In the ACD model, the behaviors of licking and biting within 35 days after modeling were significantly increased. The expression levels of Iba-1, BDNF, LCN2, GRPR, and GFAP differed significantly from those of the control group. In addition, through GEO data analyses, a strong correlation has been found between pain and IFN-γ. Similarly, in vitro experiments revealed that IFN-γ increased the expression of Iba-1, CD16, and BDNF in BV2 cells and the release of LCN2 in primary astrocytes, thus activating spinal cord glial cells. IFN-γ also induced the phosphorylation of JAK1/STAT1 and the expression of IFNGR1 in BV2 cells and primary astrocytes.</div></div><div><h3>Conclusions</h3><div>Collectively, the above findings suggest that the coexistence of chronic pain and pruritus in the ACD model is associated with the activation of spinal microglia and astrocytes. The underlying mechanism involves the binding of IFN-γ to its receptor IFNGR1, which is accompanied by the upregulation of JAK1/STAT1 signaling pathway phosphorylation.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"190 ","pages":"Pages 111-124"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146034873","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":"Corrigendum to “Neferine reduces synovial inflammation and cardiac complications in a collagen-induced arthritis mouse model via inhibiting NF-κB/NLRP3 inflammasome axis” [Mol. Immunol. 182 (2025) 117–125]","authors":"Jingjing Cao ,&nbsp;Huaxing Zhang ,&nbsp;Yanhui Ni ,&nbsp;Xiaoran Ning","doi":"10.1016/j.molimm.2026.01.004","DOIUrl":"10.1016/j.molimm.2026.01.004","url":null,"abstract":"","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"190 ","pages":"Page 110"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146034874","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":"Formononetin in Jiawei Qihuangyin inhibits podocyte epithelial–mesenchymal transition and ameliorates diabetic nephropathy via SIRT1/NF-κB axis","authors":"Huiyuan Li ,&nbsp;Jiaer Ke ,&nbsp;Yanli Zhou ,&nbsp;Huanhuan Chen ,&nbsp;Xufang Wu ,&nbsp;Huoliang Liu ,&nbsp;Juan Li","doi":"10.1016/j.molimm.2025.12.010","DOIUrl":"10.1016/j.molimm.2025.12.010","url":null,"abstract":"<div><h3>Background</h3><div>Traditional Chinese medicine (TCM) has shown great promise in treating diabetic nephropathy (DN). However, the key targets and mechanisms underlying the therapeutic effects of the active ingredients of modified prescription Jiawei Qihuangyin (JWQHY) remain unclear.</div></div><div><h3>Methods</h3><div>Network pharmacology analysis was employed to identify potential targets of JWQHY in DN. Protein–protein interaction (PPI) and TCM component–target networks were constructed, and KEGG pathway enrichment analysis was performed to determine key therapeutic targets and signaling pathways. Molecular docking suggested an interaction between the major active compound formononetin (FMN) and the central target silent information regulator 1 (SIRT1), which was experimentally validated using cellular thermal shift assay. SIRT1 expression in podocytes was assessed by qRT-PCR and western blotting (WB). Cell viability (CCK-8), apoptosis (flow cytometry), and proinflammatory cytokine secretion (ELISA) were measured to evaluate podocyte injury. The acetylation level of NF-κB p65 and epithelial–mesenchymal transition (EMT)-related proteins were analyzed by WB. In vivo, a DN rat model was established to assess the therapeutic efficacy of JWQHY through biochemical urine analysis, histopathological examination (HE staining), and WB detection of SIRT1, acetylated NF-κB p65, and EMT markers.</div></div><div><h3>Results</h3><div>Network pharmacology identified 52 potential overlapping targets of JWQHY in DN, primarily associated with the NF-κB pathway. Among these, SIRT1 was predicted and experimentally confirmed as the main target of FMN. In a high-glucose–induced podocyte injury model, FMN upregulated SIRT1 expression, promoted NF-κB p65 deacetylation, and inhibited podocyte EMT. Consistently, FMN treatment improved renal function, reduced podocyte injury, and modulated SIRT1/NF-κB signaling in DN rats.</div></div><div><h3>Conclusion</h3><div>JWQHY exerts therapeutic effects in diabetic nephropathy by modulating the SIRT1/NF-κB signaling axis through its active compound formononetin, thereby inhibiting podocyte EMT. These findings provide mechanistic insight into the pharmacological basis of FMN and support its clinical potential in DN treatment.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"190 ","pages":"Pages 1-10"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145886474","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":"Liposome-mediated simvastatin in vaccine adjuvants: Its application and mechanism","authors":"Zhijie Chen ,&nbsp;Zhiwu Xia ,&nbsp;Liping Chen ,&nbsp;Qingqing Nie ,&nbsp;Wang Gong ,&nbsp;Wenqiang Cao ,&nbsp;Xue Wang ,&nbsp;Yuehong Zou ,&nbsp;Shuai Zhang ,&nbsp;Yuchen Yang ,&nbsp;Menghong Yang ,&nbsp;Jiaming Yang ,&nbsp;Yanna Liu ,&nbsp;Lehong Zhang ,&nbsp;Wenjie Fang ,&nbsp;Yixin Chen ,&nbsp;Junlong Zhao ,&nbsp;Ziyan Meng","doi":"10.1016/j.molimm.2026.01.002","DOIUrl":"10.1016/j.molimm.2026.01.002","url":null,"abstract":"<div><div>To mitigate the APC cytotoxicity associated with simvastatin (a promising adjuvant candidate), we encapsulated this drug in liposomes to generate LIPO-SIM, and explored the potential and mechanism. Formulated via ethanol injection and rotary evaporation, liposome-SIM was characterized for appearance, ζ-average, PDI, zeta potential, and encapsulation efficiency. C57BL/6 J mice were immunized with LIPO-SIM + OVA (0/21-day schedule), euthanized on day 28 to evaluate immunogenicity, safety, and antigen presentation mechanisms. In vitro, DC2.4 cells stimulated with liposome-SIM underwent RNA-Seq, metabolomics, and western blotting to clarify adjuvant mechanisms. Results showed liposome-SIM significantly increased anti-OVA IgG titers and cellular immunity, activated local lymph node macrophages/dendritic cells, and enhanced MHC-I presentation. In vitro, AMPK inhibition and NF-κB activation were observed. No organ toxicity or inflammatory storms were detected. Liposome-SIM enhances cellular immunity via the MHC-I pathway, with AMPK/NF-κB signaling as a potential key mechanism.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"190 ","pages":"Pages 72-85"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145978735","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":"NSUN2 aggravates M1 macrophage polarization in arthritis progression through m5C modification of CCL2","authors":"Chunlei He ,&nbsp;Junhua Zhang ,&nbsp;Geer Deli ,&nbsp;Kai Zhao ,&nbsp;Lulin Liu ,&nbsp;Baojian Lai ,&nbsp;Meiyu Hu ,&nbsp;Huabin He","doi":"10.1016/j.molimm.2025.12.015","DOIUrl":"10.1016/j.molimm.2025.12.015","url":null,"abstract":"<div><h3>Background</h3><div>Arthritis is an inflammatory disease characterized by multifactorial pathogenesis in joints or surrounding tissues. M1 macrophage polarization is a key pathological feature of arthritis, and m⁵C RNA modification has been implicated in disease progression. This study aimed to elucidate the role of NSUN2, a writer of m⁵C modification, in modulating arthritis development.</div></div><div><h3>Methods</h3><div>LPS-stimulated RAW264.7 cell models and collagen-induced arthritis (CIA) rat models were established. M1 and M2 macrophage polarization was assessed by detecting cell surface markers and pro-inflammatory cytokines using immunofluorescence, enzyme-linked immunosorbent assay (ELISA), Western blot, and quantitative real-time PCR. Underlying mechanisms were investigated via methylated RNA immunoprecipitation (MeRIP), Co-immunoprecipitation (Co-IP), and Dual-Luciferase reporter assays.</div></div><div><h3>Results</h3><div>Downregulation of NSUN2 significantly inhibited M1 polarization and promoted M2 activation both <em>in vitro</em> and <em>in vivo</em>. NSUN2 enhanced m5C modification of CCL2, stabilized its mRNA expression, and facilitated its interaction with CCR2. Furthermore, NSUN2 activated the NF-κB signaling pathway in macrophages. Notably, inhibition of CCL2 activity abrogated the effects of NSUN2 on macrophage polarization.</div></div><div><h3>Conclusion</h3><div>NSUN2 drives M1 macrophage polarization through m5C modification of CCL2, thereby exacerbating arthritis progression. Targeting NSUN2 may alleviate inflammatory responses, offering a novel therapeutic strategy for arthritis treatment.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"190 ","pages":"Pages 45-55"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145928051","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":"An H₂S-releasing oridonin derivative protects HaCaT cells against metabolic stress via PI3K/AKT/Nrf2 signaling","authors":"Lang Lin ,&nbsp;Yuzhen Jia ,&nbsp;Rubing Xue ,&nbsp;Yutong Shi ,&nbsp;Dahong Li ,&nbsp;Fanxing Xu ,&nbsp;Chun Chu","doi":"10.1016/j.molimm.2025.12.012","DOIUrl":"10.1016/j.molimm.2025.12.012","url":null,"abstract":"<div><div>The chronic hyperglycemia and its-associated metabolic changes often lead to impaired wound healing, which seriously affects the quality of life of diabetic patients. Oxidative stress and apoptosis are key factors that impede epidermal cell proliferation and migration and delay wound healing. The aim of this study was to investigate the protective effect of a novel hydrogen sulfide (H₂S)-releasing oridonin derivative (OAc-Ph-ADT) on epidermal HaCaT cells against a high-glucose and high-fat environment <em>in vitro</em>. Mechanistic studies showed that OAc-Ph-ADT exerted its antioxidant effects by activating the PI3K/AKT/Nrf2 signaling pathway. Specifically, it increased PI3K and phosphorylated-AKT expression, and promotes Nrf2 nuclear translocation, which in turn enhances the mRNA and protein expression of downstream antioxidant factors (HO-1, SOD2 and NQO1). In addition, OAc-Ph-ADT significantly reduced apoptosis by inhibiting the decrease in mitochondrial membrane potential and decreasing the expression of apoptosis-related proteins (Bax, Cleaved-Caspase 3/9). It was also observed that OAc-Ph-ADT up-regulated the expression of cystathionine β-synthase (CBS) via Nrf2, which further promoted the synthesis of endogenous H₂S, resulting in positive feedback regulation. In summary, this paper elucidated through systematic <em>in vitro</em> experiments that OAc-Ph-ADT has a protective effect against epidermal cell damage in a high-glucose and high-fat environment, revealing its potential as a candidate molecule for diabetic wound treatment, and this novel H₂S-releasing oridonin derivative has a potential application as a diabetic wound healing promoter.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"190 ","pages":"Pages 21-33"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145886475","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":"Acupuncture alleviates premature ovarian insufficiency via Rictor/mTOR pathway in mice by stimulating the Guanyuan acupoint","authors":"Yu Luo ,&nbsp;Yan Chen ,&nbsp;Suning Huang ,&nbsp;Haimin Zhu ,&nbsp;Tianqi Zhao ,&nbsp;Shiyu Feng ,&nbsp;Fei Ma ,&nbsp;Yan Ning ,&nbsp;Jiaman Wu","doi":"10.1016/j.molimm.2025.12.014","DOIUrl":"10.1016/j.molimm.2025.12.014","url":null,"abstract":"<div><div>Acupuncture is a popular therapeutic therapy for premature ovarian insufficiency (POI). The specific effect and the underlying mechanism of Guanyuan acupoint on the ovarian function of POI model mice remain unclear. The female C57BL6 mice were injected peritoneally with 12 mg/kg busulfan and 120 mg/kg cyclophosphamide to induce POI. The acupuncture intervention at Guanyuan acupoint was performed on the second day after the modeling. Vaginal smears were used to monitor the estrous cycle. The hematoxylin and eosin (H&amp;E) staining was used to observe the morphological changes of ovarian tissue, and the TUNEL fluorescence staining assay was carried out to detect the apoptotic level of granulosa cells. The sex hormone levels were monitored as well. RNA sequencing was performed to select candidate gene which was regulated by acupuncture. Finally, the upstream lactating modification mechanism of Rictor was further investigated. The results showed that acupuncture at Guanyuan acupoint increased the number of vaginal exfoliated cells and inhibited the apoptosis of granulosa cell in POI model mice. Sex hormone levels indicated a marked decrease in AMH and E₂ in POI group, with a concurrent significant rise in FSH levels. Furthermore, the Rictor/mTOR pathway was inactivated in POI model group, while was prominently activated by acupuncture at Guanyuan acupoint. Acupuncture intervened H3K18la to increase Rictor promoter activity in POI. In conclusion, acupuncture at Guanyuan acupoint increased body and ovarian weight, improved ovarian tissue morphology and structure, improved follicle development, and regulated ovarian function in POI model mice. This might be related to the activation of the Rictor/mTOR pathway.</div></div>","PeriodicalId":18938,"journal":{"name":"Molecular immunology","volume":"190 ","pages":"Pages 34-44"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145928050","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}