南方医科大学学报杂志最新文献

{"title":"[A cardiac magnetic resonance-based risk prediction model for left ventricular adverse remodeling following percutaneous coronary intervention for acute ST-segment elevation myocardial infarction: a multi-center prospective study].","authors":"Zhenyan Ma, Xin A, Lei Zhao, Hongbo Zhang, Ke Liu, Yiqing Zhao, Geng Qian","doi":"10.12122/j.issn.1673-4254.2025.04.01","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.01","url":null,"abstract":"<p><strong>Objectives: </strong>To develop a risk prediction model for left ventricular adverse remodeling (LVAR) based on cardiac magnetic resonance (CMR) parameters in patients undergoing percutaneous coronary intervention (PCI) for acute ST-segment elevation myocardial infarction (STEMI).</p><p><strong>Methods: </strong>A total of 329 acute STEMI patients undergoing primary PCI at 8 medical centers from January, 2018 to December, 2021 were prospectively enrolled. The parameters of CMR, performed at 7±2 days and 6 months post-PCI, were analyzed using CVI42 software. LVAR was defined as an increase >20% in left ventricular end-diastolic volume or >15% in left ventricular end-systolic volume at 6 months compared to baseline. The patients were randomized into training (<i>n</i>=230) and validation (<i>n</i>=99) sets in a 7∶3 ratio. In the training set, potential predictors were selected using LASSO regression, followed by univariate and multivariate logistic regression to construct a nomogram. Model performance was evaluated using receiver-operating characteristic (ROC) curves, area under the curve (AUC), calibration curves, and decision curve analysis.</p><p><strong>Results: </strong>LVAR occurred in 100 patients (30.40%), who had a higher incidence of major adverse cardiovascular events than those without LVAR (58.00% <i>vs</i> 16.16%, <i>P</i><0.001). Left ventricular global longitudinal strain (LVGLS; OR=0.76, 95% <i>CI</i>: 0.61-0.95, <i>P</i>=0.015) and left atrial active strain (LAAS; OR=0.78, 95% <i>CI</i>: 0.67-0.92, <i>P</i>=0.003) were protective factors for LVAR, while infarct size (IS; OR=1.05, 95% <i>CI</i>: 1.01-1.10, <i>P</i>=0.017) and microvascular obstruction (MVO; OR=1.26, 95% <i>CI</i>: 1.01-1.59, <i>P</i>=0.048) were risk factors for LVAR. The nomogram had an AUC of 0.90 (95% <i>CI</i>: 0.86-0.94) in the training set and an AUC of 0.88 (95% <i>CI</i>: 0.81-0.94) in the validation set.</p><p><strong>Conclusions: </strong>LVGLS, LAAS, IS, and MVO are independent predictors of LVAR in STEMI patients following PCI. The constructed nomogram has a strong predictive ability to provide assistance for management and early intervention of LVAR.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"669-683"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Bioinformatics analysis of oxidative stress and immune infiltration in rheumatoid arthritis].","authors":"Zhi Gao, Ao Wu, Zhongxiang Hu, Peiyang Sun","doi":"10.12122/j.issn.1673-4254.2025.04.22","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.22","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the role of oxidative stress and immune infiltration in rheumatoid arthritis (RA).</p><p><strong>Methods: </strong>RA datasets GSE55235 (10 RA <i>vs</i> 10 normal samples) and GSE55457 (13 RA <i>vs</i> 10 normal samples) from the GEO database were merged as the test set to identify the differentially expressed genes (DEGs) in RA using R. The DEGs were intersected with oxidative stress-related genes to obtain oxidative stress-associated DEGs. KEGG and GO enrichment analyses of the DEGs were performed, and the RA-related pathways and biological processes were analyzed using GSEA. A protein-protein interaction (PPI) network was constructed using STRING and Cytoscape, and the top 10 key genes were obtained using the Degree algorithm. The validation dataset GSE1919 from GEO database was used for ROC analysis of the key genes to obtain the core genes, and their correlations with infiltrating immune cells were analyzed using CIBERSORT. The results were verified by RT-qPCR for detecting expression levels of the core genes in RA and normal joint samples.</p><p><strong>Results: </strong>We identified 89 oxidative stress-associated DEGs. Enrichment analysis suggested that these DEGs were involved in the biological processes including oxidative stress, chemical stress response, reactive oxygen species response, and lipopolysaccharide response. ROC analysis showed that the 5 core genes (STAT1, MMP9, MYC, CCL5, and JUN) all had AUC values >0.7, indicating their high diagnostic sensitivity and specificity for RA. These genes were closely correlated with immune cells, particularly T cells. RT-qPCR confirmed significant differential expressions of the core genes between RA and normal samples.</p><p><strong>Conclusions: </strong>Oxidative stress and diverse immune responses are features of RA, and the immune responses contribute to activation of oxidative stress. The identified core genes can potential serve as new diagnostic markers for RA.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"862-870"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[n-butanol fraction of ethanol extract of <i>Periploca forrestii</i> Schltr.: its active components, targets and pathways for treating Alcheimer's disease in rats].","authors":"Niandong Ran, Jie Liu, Jian Xu, Yongping Zhang, Jiangtao Guo","doi":"10.12122/j.issn.1673-4254.2025.04.14","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.14","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the active components and possible mechanisms of n-butanol fraction of <i>Periploca forrestii</i> Schltr. ethanol extract for treating Alzheimer's disease (AD).</p><p><strong>Methods: </strong>The active components of n-butanol fraction of <i>Periploca forrestii</i> Schltr. ethanol extract were analyzed using UPLC-QE-MS technique. In a SD rat model of AD induced by treatment with AlCl₃ and D-gal, the therapeutic effects of low, moderate and high doses of the n-butanol fraction, saline, and donepezil hydrochloride were evaluated using ELISA, HE and Nissl staining, immunohistochemistry and Western blotting. The therapeutic mechanisms of the n-butanol fraction were explored using network pharmacology and molecular docking.</p><p><strong>Results: </strong>Seventeen active components were identified from the n-butanol fraction of <i>Periploca forrestii</i> Schltr. ethanol extract, including phenylpropanoids, flavonoids, anthraquinones, triterpenoids, steroids, and volatile oils. In the rat models of AD, treatment with the n-butanol fraction significantly lowed AChE content in the hippocampus, increased the contents of ACh, SOD, CAT, and GSH-Px, enhanced the expressions of neuronal apoptotic factors Bcl-2, PI3K, Akt, p-PI3K, and p-Akt, and reduced the expressions of Bax and caspase-3 proteins. The treatment also dose-dependently up-regulated hippocampal expressions of Nrf-2, HO-1 and BDNF and down-regulated Keap-1, Aβ and Tau expressions. Bioinformatics analysis identified 14 key intersected targets (including TNF, AKT1 and ESR1) between the n-butanol fraction and AD.</p><p><strong>Conclusions: </strong>The therapeutic effect of n-butanol fraction of <i>Periploca forrestii</i> Schltr. ethanol extract in AD mice is mediated by its multiple active components that regulate multiple targets and pathways.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"785-798"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[A pan-cancer analysis of PYCR1 and its predictive value for chemotherapy and immunotherapy responses in bladder cancer].","authors":"Yutong Li, Xingyu Song, Ruixu Sun, Xuan Dong, Hongwei Liu","doi":"10.12122/j.issn.1673-4254.2025.04.24","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.24","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the potential of pyrroline-5-carboxylate reductase 1 (PYCR1) as a pan-cancer biomarker and investigate its expression, function, and clinical significance in bladder cancer (BLCA).</p><p><strong>Methods: </strong>Bioinformatics analysis was conducted to evaluate the associations of PYCR1 with prognosis, immune microenvironment remodeling, tumor mutation burden (TMB), and microsatellite instability (MSI) in cancer patients. Using the TCGA-BLCA dataset, univariate and multivariate regression analyses were performed to assess the potential of PYCR1 as an independent prognostic risk factor for BLCA, and a clinical decision model was constructed. The IMvigor210 cohort was utilized to evaluate the potential of PYCR1 for independently predicting the efficacy of immunotherapy. The pRRophetic was employed to screen candidate chemotherapeutic agents for treating BLCA with high PYCR1 expression. The CMap-XSum algorithm and molecular docking techniques were used to explore and validate small molecule inhibitors of PYCR1.</p><p><strong>Results: </strong>A high expression of PYCR1 was significantly associated with poor prognosis, immune cell infiltration, TMB and MSI in various tumors (<i>r</i>>0.3). PYCR1 was overexpressed in BLCA, and high PYCR1 expression was closely related to poor prognosis in BLCA patients (HR: 1.14, 95% <i>CI</i>: 1.02-1.68, <i>P</i>=0.006). The IC₅₀ of the anti-cancer drugs cetuximab, 5-fluorouracil, and doxorubicin increased significantly in BLCA cell lines with high PYCR1 expressions (<i>P</i><0.0001).</p><p><strong>Conclusions: </strong>High PYCR1 expression is an independent risk factor for poor prognosis in BLCA patients and can serve as a significant indicator for clinical decision-making as well as a marker for predicting sensitivity to chemotherapeutic agents and the efficacy of immunotherapy.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"880-892"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144036322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Catalpol reduces liver toxicity of triptolide in mice by inhibiting hepatocyte ferroptosis through the SLC7A11/GPX4 pathway: testing the <i>Fuzheng Zhidu</i> theory for detoxification].","authors":"Linluo Zhang, Changqing Li, Lingling Huang, Xueping Zhou, Yuanyuan Lou","doi":"10.12122/j.issn.1673-4254.2025.04.16","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.16","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the protective effect of catalpol against triptolide-induced liver injury and explore its mechanism to test the <i>Fuzheng Zhidu</i> theory for detoxification.</p><p><strong>Methods: </strong>C57BL/6J mice were randomized into blank control group, catalpol group, triptolide group and triptolide+catalpol group. After 13 days of treatment with the agents by gavage, the mice were examined for liver tissue pathology, liver function, hepatocyte subcellular structure, lipid peroxidation, ferrous ion deposition and expressions of ferroptosis-related proteins in the liver. In a liver cell line HL7702, the effect of catalpol or the ferroptosis inhibitor Fer-1 on triptolide-induced cytotoxicity was tested by examining cell functions, Fe²⁺ concentration, lipid peroxidation, ROS level and the ferroptosis-related proteins.</p><p><strong>Results: </strong>In C57BL/6J mice, catalpol significantly alleviated triptolide-induced hepatic injury, lowered the levels of ALT, AST and LDH, and reversed the elevation of Fe²⁺ concentration and MDA level and the reduction of GP_X level. In HL7702 cells, inhibition of ferroptosis by Fer-1 significantly reversed triptolide-induced elevation of ALT, AST and LDH levels. Western blotting and qRT-PCR demonstrated that catalpol reversed abnormalities in expressions of SLC7A11, FTH1 and GPX4 at both the mRNA and protein levels in triptolide-treated HL7702 cells.</p><p><strong>Conclusions: </strong>The combined use of catalpol can reduce the hepatotoxicity of triptolide in mice by inhibiting excessive hepatocyte ferroptosis through the SLC7A11/GPX4 pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"810-818"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144002190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Moslosooflavone ameliorates dextran sulfate sodium-induced colitis in mice by suppressing intestinal epithelium apoptosis <i>via</i> inhibiting the PI3K/AKT signaling pathway].","authors":"Fei Chu, Xiaohua Chen, Bowen Song, Jingjing Yang, Lugen Zuo","doi":"10.12122/j.issn.1673-4254.2025.04.17","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2025.04.17","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effect of moslosooflavone (MOS) for ameliorating dextran sulfate sodium (DSS)-induced colitis in mice and the underlying molecular mechanism.</p><p><strong>Methods: </strong>C57BL/6J mice with or without DSS exposure in the drinking water were both randomized into two groups for treatment with intraperitoneal injections with MOS (200 mg/kg) or normal saline for 7 days (<i>n</i>=6). Disease severity of the mice was assessed by observing changes in body weight, colon length, histopathology (HE staining), intestinal barrier function, and TUNEL staining. In the <i>in vitro</i> studies, lipopolysaccharide (LPS)-stimulated mouse colon organoids were treated with MOS (120 μmol/L) for 24 h, and the changes in barrier dysfunction and inflammation were analyzed. Network pharmacology and Western blotting were employed to identify functional pathways and apoptotic protein regulation associated with the therapeutic effect of MOS on colitis.</p><p><strong>Results: </strong>In the mouse models of DSS-indcued colitis, MOS treatment significantly reduced body weight loss, disease activity index (DAI) scores and colon shortening, ameliorated colonic histopathological changes and inflammation, and lowered pro-inflammatory cytokine levels (TNF-α, IL-1β, IL-6, and IFN-γ). MOS effectively restored intestinal barrier integrity in the mice by reducing serum FITC-dextran and I-FABP concentrations while enhancing the tight junction proteins (ZO-1 and claudin-1). In the colon organoids, MOS significantly suppressed LPS-induced inflammatory responses and epithelial barrier disruption. Western blotting revealed that MOS downregulated C-caspase-3 and BAX and upregulated Bcl-2 expressions in both models. Mechanistically, MOS suppressed PI3K and AKT phosphorylation in both DSS-treated mouse colonic tissues and LPS-stimulated organoids.</p><p><strong>Conclusions: </strong>MOS alleviates experimental colitis in mice by inhibiting intestinal epithelial apoptosis via inhibiting the PI3K/AKT pathway, thereby restoring intestinal barrier integrity and reducing inflammation.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 4","pages":"819-828"},"PeriodicalIF":0.0,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The splicing factor HNRNPH1 regulates Circ-MYOCD back-splicing to modulate the course of cardiac hypertrophy].","authors":"Rui Cai, Zhuo Huang, Wenxia He, Tianhong Ai, Xiaowei Song, Shuting Hu","doi":"10.12122/j.issn.1673-4254.2025.03.16","DOIUrl":"10.12122/j.issn.1673-4254.2025.03.16","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the mechanism of Circ-MYOCD back-splicing and its regulatory role in myocardial hypertrophy.</p><p><strong>Methods: </strong>Sanger sequencing and RNase R assays were performed to verify the circularity and stability of Circ-MYOCD, whose subcellular distribution was determined by nuclear-cytoplasmic fractionation. Bioinformatics analysis and mass spectrometry from pull-down assays were conducted to predict the RNA-binding proteins (RBPs) interacting with Circ-MYOCD. In rat cardiomyocytes H9C2 cells, the effects of HNRNPH1 and HNRNPL knockdown and overexpression on Circ-MYOCD back-splicing were evaluated. In a H9C2 cell model of angiotensin II (Ang II)-induced myocardial hypertrophy, the expression of HNRNPH1 was detected, the effects of HNRNPH1 knockdown and overexpression on progression of myocardial hypertrophy were assessed, and the regulatory effect of HNRNPH1 on Circ-MYOCD back-splicing was analyzed.</p><p><strong>Results: </strong>Sanger sequencing confirmed that the junction primers could amplify the correct Circ-MYOCD sequence. RNase R and nuclear-cytoplasmic fractionation assays showed that Circ-MYOCD was stable and predominantly localized in the cytoplasm. Bioinformatics analysis and mass spectrometry from the Circ-MYOCD pull-down assay identified HNRNPH1 and HNRNPL as the RBPs interacting with Circ-MYOCD. In H9C2 cells, HNRNPH1 knockdown significantly enhanced while its overexpression inhibited Circ-MYOCD back-splicing; HNRNPH1 overexpression obviously increased the expressions of myocardial hypertrophy markers ANP and BNP, while its knockdown produced the opposite effect. In Ang II-induced H9C2 cells, which exhibited a significant increase of HNRNPH1 expression and increased expressions of ANP and BNP, HNRNPH1 knockdown obviously increased Circ-MYOCD expression, decreased MYOCD expression and lowered both ANP and BNP expressions.</p><p><strong>Conclusions: </strong>HNRNPH1 regulates Circ-MYOCD back-splicing to influence the progression of myocardial hypertrophy.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 3","pages":"587-594"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[CEACAM6 inhibits proliferation and migration of nasopharyngeal carcinoma cells by suppressing epithelial-mesenchymal transition].","authors":"Lu Tao, Zhuoli Wei, Yueyue Wang, Ping Xiang","doi":"10.12122/j.issn.1673-4254.2025.03.14","DOIUrl":"10.12122/j.issn.1673-4254.2025.03.14","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate CEACAM6 expression in nasopharyngeal carcinoma (NPC) and its regulatory effects on tumor cell proliferation, migration, and epithelial-mesenchymal transition (EMT).</p><p><strong>Methods: </strong>CEACAM6 expression in NPC was analyzed using GEO datasets and validated by immunohistochemistry in NPC tissues and by Western blotting and RT-qPCR in NPC cell lines (HNE1, C666-1, HK1, 5-8F and CNE2Z) and normal nasopharyngeal epithelial NP69 cells. In the NPC cell lines, the effects of lentivirus-mediated CEACAM6 overexpression and knockdown on cell proliferation, migration, invasion and cytoskeletal structures were evaluated using CCK-8 assay, Edu staining, wound healing assay, Transwell assay, and phalloidin staining. Western blotting was performed to determine the expressions of EMT-related proteins (FN1, ITGA5, ITGB1, E-cadherin, N-cadherin and vimentin) in the NPC cells and the effect of FN1 overexpression on ITGA5 and ITGB1 protein expressions.</p><p><strong>Results: </strong>Analysis of the data from the GEO datasets suggested that CEACAM6 was significantly downregulated in NPC, which was associated with poor patient prognosis. Immunohistochemistry also showed low expressions of CEACAM6 in clinical NPC tissues (<i>P</i><0.05). In NPC cells, CEACAM6 overexpression significantly suppressed cell proliferation, migration and invasion and reduced the fluorescence intensity of actin. CEACAM6 overexpression also resulted in significant downregulation of FN1, ITGA5, ITGB1, N-cadherin and vimentin expressions and upregulation of E-cadherin expression, and FN1 overexpression obviously attenuated the inhibitory effect of CEACAM6 overexpression on ITGA5 and ITGB1 expressions.</p><p><strong>Conclusions: </strong>CEACAM6 inhibits NPC cell migration and invasion by inhibiting EMT via regulating FN1, ITGA5 and ITGB1 expressions.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 3","pages":"566-576"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[<i>Didang</i> Decoction-medicated serum enhances autophagy in high glucose-induced rat glomerular endothelial cells <i>via</i> the PI3K/Akt/mTOR signaling pathway].","authors":"Yanyan Dong, Kejing Zhang, Jun Chu, Quangen Chu","doi":"10.12122/j.issn.1673-4254.2025.03.03","DOIUrl":"10.12122/j.issn.1673-4254.2025.03.03","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effect of <i>Didang</i> Decoction-medicated serum on autophagy in high glucose (HG)-induced rat glomerular endothelial cells (RGECs) and explore the pathway that mediates its effect.</p><p><strong>Methods: </strong>Primary RGECs were isolated and cultured using sequential sieving combined with collagenase digestion, followed by identification using immunofluorescence assay for factor VIII. High glucose medium was used to induce RGECs to simulate a diabetic environment, and the effects of <i>Didang</i> Decoction-medicated serum and 3-MA (an autophagy inhibitor), either alone or in combination, on autophagy of HG-exposed cells were evaluated by observing autophagic vacuoles using monodansylcadaverine (MDC) staining. RT-qPCR and Western blotting were employed to measure mRNA and protein expression levels of Beclin-1, p62, LC3B, p-PI3K, p-Akt, and p-mTOR.</p><p><strong>Results: </strong>Compared with the control cells, the HG-exposed RGECs showed significantly reduced autophagic fluorescence intensity, decreased Beclin-1 mRNA expression, increased p62 mRNA expression, downregulated Beclin-1 protein and LC3-II/I ratio, and upregulated p62, p-PI3K, p-Akt, and p-mTOR protein levels. <i>Didang</i> Decoction-medicated serum significantly enhanced autophagic fluorescence intensity in HG-exposed cells, increased Beclin-1 mRNA expression, decreased p62 mRNA expression, upregulated Beclin-1 protein, and downregulated p62, p-PI3K, p-Akt, and p-mTOR protein levels.</p><p><strong>Conclusions: </strong><i>Didang</i> Decoction-medicated serum enhances autophagy in HG-exposed RGECs by regulating the PI3K/Akt/mTOR signaling pathway, which sheds light on a new therapeutic strategy for diabetic nephropathy.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 3","pages":"461-469"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955890/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[High expression of hexokinase 2 promotes proliferation, migration and invasion of colorectal cancer cells by activating the JAK/STAT pathway and regulating tumor immune microenvironment].","authors":"Shunjie Qing, Zhiyong Shen","doi":"10.12122/j.issn.1673-4254.2025.03.12","DOIUrl":"10.12122/j.issn.1673-4254.2025.03.12","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the expression of hexokinase 2 (HK2) in colorectal cancer (CRC) and its possible mechanisms for regulating tumor cell behaviors and tumor immune microenvironment.</p><p><strong>Methods: </strong>We analyzed HK2 expression in CRC and its impact on patient prognosis and tumor immune microenvironment using public databases. HK2 expression was also examined in 8 CRC and paired adjacent tissues using immunohistochemistry, Western blotting and RT-qPCR. In cultured CRC cell lines CT26 and HCT116 with low HK2 expression, the effects of lentivirus-mediated HK2 overexpression and JAK/STAT3 inhibitors on cell proliferation, migration, and invasion were assessed using CCK-8 assay, colony formation assay and Transwell assay and in a subcutaneous tumor-bearing mouse model; the changes were also observed in MC38 and CACO2 cells with high HK2 expressions following treatment with HK2 inhibitor 3-BP. Western blotting was performed to verify the relationship between HK2 and JAK/STAT signaling pathway protein expressions.</p><p><strong>Results: </strong>Informatics analyses suggested that HK2 expression was significantly higher in CRC tissues than in adjacent tissues (<i>P</i><0.001), and patients with high HK2 expressions had worse prognosis (<i>P</i>=0.09). In the 8 clinical CRC tissues, HK2 expressions were significantly higher in the tumor tissues than in the adjacent tissues (<i>P</i><0.01). In CT26 and HCT116 cells, HK2 overexpression significantly enhanced cell proliferation, migration and invasion, while in HK2-overexpressing MC38 and CACO2 cells, inhibiting HK2 with 3-BP strongly suppressed these changes. HK2 overexpression promoted STAT3 phosphorylation, and JAK/STAT3 inhibitors effectively suppressed tumor cell proliferation, migration and invasion. TIMER and MCPcounter analyses indicated correlations between HK2 and immune cells, and TCGA and GEO analyses suggested significant positive correlations between HK2 and the immune checkpoints including PDCD1.</p><p><strong>Conclusions: </strong>HK2 is upregulated in CRC to promote tumor cell proliferation, migration and invasion possibly by activating the JAK-STAT signaling pathway and modulating tumor immune microenvironment.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 3","pages":"542-553"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}