细胞与分子免疫学杂志最新文献

{"title":"[The role of macrophage efferocytosis in non-infectious inflammatory diseases].","authors":"Xingyu Lu, Yujing Xiong, Xin Zhao, Guojun Gao, Yongli Hou, Lihua Chen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Macrophages play a critical role in maintaining tissue homeostasis and regulating inflammation through the efficient clearance of apoptotic cells, a process known as efferocytosis. Defective macrophage efferocytosis has been identified as a significant mechanism underlying persistent inflammation and tissue damage in various non-infectious inflammatory diseases (NIID), including atherosclerosis (AS), systemic lupus erythematosus (SLE), and inflammatory bowel disease (IBD), etc. Impaired efferocytosis not only leads to the accumulation of apoptotic cells and secondary necrosis, triggering the release of inflammatory signals, but also disrupts immune tolerance and tissue repair processes. Recent advances in understanding the mechanisms of efferocytosis, encompassing apoptotic cell recognition, receptor regulation, and anti-inflammatory responses, have revealed novel therapeutic opportunities. This review summarizes the mechanistic roles of macrophage efferocytosis in NIID, discusses its potential as both a therapeutic target and a biomarker, and outlines future directions in molecular mechanisms, tissue-specific immunoregulation, and clinical translation.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 3","pages":"245-251"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147610683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Study on the regulation mechanism of IL-17 signaling pathway and its intervention strategy in inflammatory diseases].","authors":"Yang Liu, Yingying Chen, Ziru Wei, Xiaolin Zhang, Hongchun Zhao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The interleukin 17 (IL-17) signaling pathway plays a crucial role in the pathogenesis of various inflammation-related diseases and tumours. The IL-17 family of cytokines, particularly IL-17A, has been extensively studied, revealing its pro-inflammatory effects and dual-role in immune responses. Recent studies have shown that IL-17 not only promotes the progression of autoimmune diseases such as psoriasis and ankylosing spondylitis but also facilitates tumour development by regulating immune escape mechanisms within the tumour microenvironment. Although therapeutic strategies targeting IL-17 have shown promising clinical potential, the differences in their effects across various patients and disease states require further investigation. This review will discuss the biological functions of the IL-17 signaling pathway, its dual-role in various diseases, as well as the challenges posed by current targeted therapies and future research directions.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 3","pages":"252-258"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147610708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[PD-L1 expression in primary non-small cell lung cancer and paired brain metastasis: consistency and clinical implications].","authors":"Jiamin Liang, Na Ning, Fuqin Zhang, Lanlan Feng, Qiao Liu, Jiao Ma, Yan Zhang, Dongjing Ding, Xiujuan Han, Shaojun Zhu, Li Gong, Wei Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To investigate the concordance of programmed death ligand-1 (PD-L1) expression between primary non-small cell lung cancer (NSCLC) and paired brain metastasis, analyze its relationship with clinicopathological characteristics, and evaluate the feasibility of using primary tumor PD-L1 status to predict brain metastasis status. Methods Thirty-two paired primary NSCLC and brain metastasis samples, pathologically diagnosed between January 1, 2017 and July 1, 2022, were collected. PD-L1 expression was detected by immunohistochemistry and interpreted using the Tumor Proportion Score (TPS), with cut-off values set at 1% and 50%. The Chi-square test was used to analyze the relationship between PD-L1 expression and clinicopathological features. Paired Chi-square and Kappa consistency tests were employed to assess the concordance of PD-L1 expression between primary and metastatic sites. Results PD-L1 expression showed no significant correlation with patient gender, age, treatment history, or histologic type. At the 1% cut-off, the overall PD-L1 expression showed moderate concordance between primary and metastatic sites (Kappa=0.624). Subgroup analysis revealed high concordance in untreated patients (Kappa=0.761, P=0.001), whereas the treated group showed weak concordance without statistical significance (Kappa=0.324, P=0.205). At the 50% cut-off, both the treatment group and the untreated group showed weak concordance without statistical significance. Although the chemotherapy subgroup showed perfect agreement (Kappa=1.000) at the 50% cut-off, the high-expression concordance rate was only 20.00%, indicating limited clinical reference value. Conclusion The strong concordance of PD-L1 expression in the untreated group patients supports the use of primary tumor PD-L1 status to guide clinical decision-making when brain metastasis tissue is unavailable. Treatment status (mainly including chemotherapy) may be an important factor affecting the consistency of high PD-L1 expression between primary NSCLC and brain metastasis.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 3","pages":"230-236"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147610668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The effect of plasma exchange on immune function in patients with hyperbilirubinemia at different severity levels following liver cancer surgery].","authors":"Chunyun Zeng, Lu Sun, Ruchun Wen, Yuting Wu","doi":"","DOIUrl":"","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Objective To analyze the effect of plasma exchange on immune function in patients with hyperbilirubinemia of different severity after liver cancer surgery. Methods A total of 100 patients diagnosed with hyperbilirubinemia following liver cancer resection at Ganzhou People's Hospital from January 1, 2021 to December 31, 2024 were enrolled as the study participants. Using a random number table, they were assigned to either a control group (conventional drug therapy, n=50) or an observation group (conventional drug therapy+plasma exchange therapy, n=50). All patients were further categorized by hyperbilirubinemia severity as mild, moderate, or severe. The distribution within the control group was 12 (mild), 25 (moderate), and 13 (severe); the distribution within the observation group was 14 (mild), 24 (moderate), and 12 (severe). Fasting venous blood samples were collected from all participants to assess immune function and other indicators. Generalized estimating equation (GEE) models were used to analyze the differences in immune function indicators across different severity levels and between the two groups before and after treatment, as well as the interactive effects of time point, group, and disease severity on the relevant scores. Results Compared with the pre-treatment levles, the immune, liver, and coagulation function indicators in both groups were significantly improved after treatment. Before treatment, as hyperbilirubinemia severity increased from mild to severe, levels of immunoglobulin A (IgA), immunoglobulin G (IgG), immunoglobulin M (IgM), the Child-Pugh score for liver function, and the albumin-bilirubin (ALBI) score showed an upward trend, while the CD4&lt;sup&gt;+&lt;/sup&gt;/CD8&lt;sup&gt;+&lt;/sup&gt; ratio showed a downward trend in both groups. After treatment, this trend persisted in both the control group and the observation group. Post-treatment comparisons between patients of the same severity level in the two groups showed that the observation group had significantly lower IgA, IgG, IgM, Child-Pugh, and ALBI score, and a significantly higher CD4&lt;sup&gt;+&lt;/sup&gt;/CD8&lt;sup&gt;+&lt;/sup&gt; ratio than the control group. Furthermore, the magnitude of improvement in coagulation, liver, and immune function indicators was significantly greater in the observation group across all severity levels. The total clinical effectiveness rate was significantly higher in the observation group. GEE analysis showed that the levels of IgA, IgG, and IgM were significantly increased, while the CD4&lt;sup&gt;+&lt;/sup&gt;/CD8&lt;sup&gt;+&lt;/sup&gt; ratio was significantly decreased with the increase in the severity of hyperbilirubinemia. The levels of IgA, IgG, and IgM were significantly decreased and the CD4&lt;sup&gt;+&lt;/sup&gt;/CD8&lt;sup&gt;+&lt;/sup&gt; ratio was significantly increased after treatment. The decline in IgA, IgG, and IgM levels in the observation group was greater than that in the control group, and the increase in the CD4&lt;sup&gt;+&lt;/sup&gt;/CD8&lt;sup&gt;+&lt;/sup&gt; ratio was also greater. The observation group demon","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 2","pages":"148-158"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[SOX4 drives the differentiation of CD4⁺T cells toward an immunosuppressive phenotype].","authors":"Yuelu Zhang, Ziqi Tao, Xi Huang, Zhijie Liu, Yiyang Dong, Lingfei Zhou, Menghui Huang, Fang Wang","doi":"","DOIUrl":"","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Objective To investigate the regulatory effects of the SRY-box transcription factor 4 (SOX4) on differentiation and oxidative phosphorylation (OXPHOS) metabolism of CD4&lt;sup&gt;+&lt;/sup&gt;T cells. Methods CD4&lt;sup&gt;+&lt;/sup&gt;T cells were isolated from healthy human peripheral blood using magnetic bead sorting. After stimulation with CD3 and CD28 antibodies for two days, CD4&lt;sup&gt;+&lt;/sup&gt;T cells were infected with lentivirus to establish the SOX4-overexpression (SOX4-OE) group and the empty vector (Vector) group, respectively. Flow cytometry was used to analyze the expression of phenotypic markers [CD25, programmed cell death protein 1 (PD-1), cytotoxic lymphocyte antigen 4 (CTLA-4), glucocorticoid-induced tumor necrosis factor receptor (GITR), tumor necrosis factor receptor superfamily member 4 (OX-40)], the transcription factor forkhead box P3 (FOXP3), intracellular cytokines [transforming growth factor β1(TGF-β1), interleukin 10(IL-10), interferon γ(IFN-γ), IL-4, IL-17A ], and OXPHOS-related indicators [adenosine triphosphate (ATP), reactive oxygen species (ROS), mitochondrial reactive oxygen species (mtROS), mitochondrial mass, mitochondrial respiratory chain complexes] in CD4&lt;sup&gt;+&lt;/sup&gt;T cells from the SOX4-OE group and the Vector group. RNA sequencing was conducted to identify differentially expressed genes (DEGs) between the SOX4-OE and Vector groups, followed by enrichment analyses on the identified DEGs including Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), and GeneSet Enrichment Analysis (GSEA). Results Compared to the Vector group, the SOX4-OE group exhibited significantly increased proportions of CD4&lt;sup&gt;+&lt;/sup&gt;T cells expressing the activation markers CD25 and GITR, as well as the inhibitory molecules CTLA-4 and PD-1, while the proportion of cells expressing OX-40 remained unchanged between the two groups. The transcription factor FOXP3 was significantly upregulated in SOX4-OE CD4&lt;sup&gt;+&lt;/sup&gt;T cells compared to the Vector group. Regarding intracellular cytokines, the proportions of CD4&lt;sup&gt;+&lt;/sup&gt;T cells producing TGF-β1, IFN-γ, and IL-17A were significantly higher in the SOX4-OE group than in the Vector group. Conversely, the proportion of IL-10-producing cells was significantly lower, while no significant difference was observed for IL-4. RNA sequencing analysis of DEGs in CD4&lt;sup&gt;+&lt;/sup&gt;T cells from the SOX4-OE and Vector groups revealed significant enrichment of the OXPHOS pathway via KEGG pathway analysis. GO enrichment analysis indicated that DEGs were significantly enriched in terms of immune response regulation, aerobic electron transport chain, and positive regulation of TGF-β production. GSEA showed that, compared with the Vector group, SOX4-OE CD4&lt;sup&gt;+&lt;/sup&gt;T cells exhibited upregulation in the TGF-β receptor complex-mediated signaling pathway and in the transcriptional activity of Sma and Mad homolog 2 (SMAD2)/SMAD3: SMAD4 heterotrimer complex. Moreover, SOX4 overexpression enhanced ATP production and the l","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 2","pages":"97-105"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research progress on the role of myeloid-derived suppressor cells in multiple sclerosis].","authors":"Xuying Zhao, Jiaqi Ding, Renle Ren, Jun Guo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of cells composed of myeloid progenitor cells, immature granulocytes, monocytes, and dendritic cells. These cells were initially discovered in cancer research and have been confirmed to show immunosuppressive functions. In recent years, their role in autoimmune diseases has attracted more attention. Multiple sclerosis (MS) is a rare autoimmune disease of the central nervous system, which can lead to non-traumatic disability among young adults. However, the exact pathogenesis is still unclear, and there is no therapy to cure MS. Studies have shown that MDSCs can play an important immunomodulatory role in MS and experimental autoimmune encephalomyelitis (EAE) model through multiple pathways. This article reviews the origin and characteristics of MDSCs and their role in MS/EAE, with the aim of proposing new strategies for investigating the pathogenesis and treatment of MS.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 2","pages":"159-163"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The role of monocytes in Hantaan virus-induced vascular endothelial injury using a co-culture model].","authors":"Yanbo Wang, Yue Si, Tingwei Jia, Yunle Wang, Hongwei Ma, Linfeng Cheng, Fanglin Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To investigate the role and regulatory mechanism of monocytes in the dysfunction of vascular endothelial cell induced by Hantaan virus(HTNV) infection. Methods The in vitro co-culture model based on Transwell chambers was established [Human umbilical vein endothelial cells (HUVECs) were seeded in the middle layer, Human embryonic kidney cell 293 (HEK293) cells in the lower layer, and peripheral blood mononuclear cells(PBMCs) or monocyte-depleted PBMCs in the upper layer]. The monocytes in PBMCs were removed by the adherent method and the efficiency of removal was verified by flow cytometry (FCM). The expression of HTNV nucleocapsid protein (NP) in tissue cells was detected by Western blot to evaluate the effects of monocytes on viral replication. The levels of cytokine secretion and the states of T cell activation in the co-culture model were detected by Bio Plex suspension chip system and FCM, respectively. Finally, HUVEC permeability was assessed by measuring transepithelial electrical resistance (TER) following monocyte depletion or the addition of an anti-tumor necrosis factor α (TNF-α) neutralizing antibody. This was designed to determine whether monocytes exacerbate endothelial injury after HTNV infection by disrupting immune microenvironment homeostasis. Results Depletion of monocytes significantly increased HTNV NP expression in both HEK293 cells and HUVECs. Concurrently, levels of pro-inflammatory cytokines, including TNF-α, interleukin 1β(IL-1β), and IL-6, in the upper chamber culture medium were significantly reduced. Furthermore, the activation of cytotoxic T lymphocytes (CTL), type 1 helper T(Th1), Th2, and Th17 cells in the PBMCs was inhibited. The decline in the transepithelial electrical resistance of HUVEC was attenuated following monocyte removal, and this monocyte-mediated increase in endothelial permeability was reversed by the anti-TNF-α neutralizing antibody. Conclusion In this study, the methodology of the Transwell experiment is improved, allowing a better simulation of the in vivo process of HTNV infection. The findings reveal a dual regulatory role of monocytes in HTNV-induced vascular endothelial cell injury. Monocytes could not only inhibit HTNV replication but also promote T cell activation and increase vascular endothelial permeability through the secretion of pro-inflammatory cytokines such as TNF-α. Intervention targeting TNF-α significantly alleviate endothelial cell injury caused by HTNV infection.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 2","pages":"106-114"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[A network pharmacology-based study to explore the mechanism of a novel sleep-aiding soup for the treatment of insomnia by modulating microglia activation].","authors":"Zhen Wu, Zhuoqiong Bian, Ailin Chen, Qiuping Zhang, Jie Li, Hui Zhou, Hongying Zhu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective Building on prior clinical evidence demonstrating the efficacy of a novel sleep-aid decoction in treating insomnia among elderly patients, this study aimed to explore its potential mechanism of action by integrating network pharmacology with in vitro experiments, with a focus on microglial activation regulation. Methods Active compounds and potential targets of the decoction were identified using the TCMSP and HERB databases. These targets were then intersected with insomnia-and microglial activation-related targets to construct a protein-protein interaction (PPI) network. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted via the DAVID platform to identify key signaling pathways. An in vitro model of microglial activation was established by stimulating BV2 cells with lipopolysaccharide (LPS). The effects of the decoction-containing serum on inflammatory cytokine levels and microglial activation markers were assessed using ELISA, quantitative real-time PCR (qRT-PCR), and nitric oxide (NO) assays. Results A total of 87 active compounds and 831 predicted targets were identified, including 62 overlapping targets associated with insomnia and microglial activation. PPI and pathway analyses indicated significant enrichment in classical neuroinflammation-related pathways, including the advanced glycation end product-receptor for advanced glycation end product (AGE-RAGE), Toll-like receptor (TLR), Janus kinase/signal transducer and activator of transcription (JAK/STAT), and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathways. In vitro experiments showed that the decoction-containing serum significantly suppressed LPS-induced expression of interleukin 1β (IL-1β), IL-6, tumor necrosis factor α (TNF-α), and NO, while downregulating both mRNA and protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2). These results indicated effective inhibition of microglial activation and inflammatory responses. Conclusion The novel sleep-aid decoction may alleviate insomnia by modulating the AKT signaling pathway, thereby suppressing proinflammatory microglial polarization and reducing neuroinflammation. This study reveals a potential immunomodulatory mechanism of this traditional Chinese medicine formula and highlights the value of its multi-component, multi-target approach for sleep disorder management. Further studies integrating multi-omics and single-cell technologies are warranted to elucidate the specific roles and targets of its key active components.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 2","pages":"122-128"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The mechanism of the effect of GalNAc-T4 on the mitochondrial autophagy of the injury of H9c2 cardiomyocytes induced by hypoxia/reoxygenation under high glucose environment via extracellular signal regulated kinase 1/2 signaling pathway].","authors":"Dayou Ding, Guangrong Zhao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To investigate the effect of N-acetylglucosamine transferase 4 (GalNAc-T4) on the mitochondrial autophagy in H9c2 cell injury model induced by hypoxia/reoxygenation (H/R) in high glucose (HG) environment, and its regulatory mechanism on extracellular signal regulated kinase 1/2 (ERK1/2) signaling pathway. Methods The cell experiments were divided into five groups. Control group (Control): Cells were transfected with pc-NC cells. HG group: 50 mmol/L glucose was added to the culture medium, and cells were transfected with pc-NC. HG+H/R group: In addition to the HG treatment, cells were subjected to a low oxygen environment for 6 hours, followed by transfection with the pc-NC vector. Overexpression group (pc): Cells were transfected with the pc while undergoing HG+H/R treatment. ERK1/2 agonist epidermal growth factor (EGF) group: Cells were treated with HG+H/R and transfected with the pc, supplemented with 20 ng/mL EGF in the culture medium. The proliferation activity, apoptosis rate, mitochondrial membrane potential, the levels of reactive oxygen species (ROS), iron ions, and mitochondrial autophagy in each group of cells were detected. The expressions of GalNAc-T4, ERK1/2, phosphorylated ERK1/2 (p-ERK1/2), translocase of outer mitochondrial membrane 20 (TOM20), translocase of inner mitochondrial membrane 23 (TIM23), B cell lymphoma 2 (Bcl2), and Bcl2 associated X protein (BAX) were detected in cells. Results Overexpression of GalNAc-T4 significantly increased the proliferation activity, the mitochondrial membrane potential, and the expression of TOM20, TIM23, and Bcl2 in H9c2 cells in HG+H/R group, and decreased the cell apoptosis rate, the levels of ROS and iron ion. Meanwhile, it inhibited the mitochondrial autophagy and downregulated the expression of p-ERK1/2/ERK1/2 and BAX in cells. EGF partially reversed the protective effect of the overexpression of GalNAc-T4 on cardiomyocytes, and the differences were statistically significant. Conclusion Overexpression of GalNAc-T4 could significantly improve the mitochondrial dysfunction in H9c2 cells undergoing hypoxia/reoxygenation under high glucose conditions, inhibit oxidative stress and excessive mitochondrial autophagy, and reduce the apoptosis rate of cardiomyocytes. This may be related to its ability to block the activation of ERK1/2 signaling pathway.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 2","pages":"129-139"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Anti-Chlamydia trachomatis activity and underlying mechanisms of baicalin in vitro].","authors":"Silu Gong, Yan Zou, Rong Yu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Objective To examine the inhibitory effect of baicalin on Chlamydia trachomatis (C.trachomatis) activity and its impact on pyroptosis in infected cells in vitro. Methods A cell model of C.trachomatis infection was established. The effects of various concentrations of baicalin on C.trachomatis inclusion bodies and infectious progeny were assessed. Cell viability was measured using the CCK-8 assay to determine the optimal non-cytotoxic concentration of baicalin for subsequent experiments. The time-dependent inhibitory effect of baicalin was analyzed using a drug withdrawal protocol. Cellular morphology was observed under an inverted phase-contrast microscope to detect pyroptotic features. The expression levels of pyroptosis-related proteins NLRP3, pro-caspase-1, cleaved-caspase-1, gasdermin D-N(GSDMD-N), and gasdermin E (GSDME) in C.trachomatis-infected cells were measured by Western blot. Results Baicalin inhibited C.trachomatis growth in a concentration-dependent manner. CCK-8 assays indicated that baicalin, at concentrations as high as 90 μmol/L, had no significant effect on host cell viability (>90%). The anti-chlamydial activity of baicalin was also time-dependent. Inverted microscopy revealed that C.trachomatis-infected cells exhibited characteristic pyroptotic morphology, including cell swelling and bubble-like protrusions, which were markedly attenuated by baicalin treatment. Western blot analysis revealed that baicalin markedly suppressed the protein expression levels of NLRP3, pro-caspase-1, cleaved-caspase-1, GSDMD-N, and GSDME in C.trachomatis-infected cells. Conclusion Baicalin effectively inhibits C.trachomatis growth in vitro. The underlying mechanism may be associated with the modulation of pyroptosis pathways mediated by both the NLRP3/caspase-1/GSDMD axis and GSDME.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 2","pages":"115-121"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}