南方医科大学学报杂志最新文献

{"title":"[Hollow copper sulfide nanocomposites combined with photothermal and photodynamic therapy inhibits malignant behaviors of esophageal cancer cells].","authors":"Pingjuan Yang, Anqi Ji, Shuxin Liao, Haonan Yao, Zhendong Gao, Pan Chen, Haoyan Cheng, Shegan Gao, Linlin Shi","doi":"10.12122/j.issn.1673-4254.2026.04.13","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.13","url":null,"abstract":"<p><strong>Objectives: </strong>To develop a hollow Cu₉S₈-based nanoparticles loaded with the photosensitizer IR780, investigate its photothermal and photodynamic (PTT-PDT) effects against esophageal cancer cells and analyze the underlying mechanisms.</p><p><strong>Methods: </strong>Hollow Cu₉S₈ nanoparticles were synthesized using a sacrificial-template strategy, and IR780 was encapsulated within a lauric acid matrix to serve as a phase-change material for preparing IR780@Cu₉S₈ composite nanoparticles. The composite nanoparticles were characterized for morphology and structural attributes using transmission electron microscopy, X-ray diffraction, and UV-visible spectroscopy. The effects of IR780@Cu₉S₈ on proliferation, invasion, and migration of esophageal cancer cells under near-infrared (NIR) irradiation (808 nm, 1.5 W/cm², 5 min) were assessed using CCK-8 assay, live/dead staining, reactive oxygen species, mitochondrial membrane potential assay, wound-healing assay, and Transwell assay. The <i>in vivo</i> PTT-PDT therapeutic efficacy and biosafety of IR780@Cu₉S₈ was evaluated in a mouse model bearing subcutaneous esophageal cancer xenografts.</p><p><strong>Results: </strong>The synthesized IR780@Cu₉S₈ nanoparticles exhibited a uniform quasi-spherical morphology with a photothermal conversion efficiency of 44.0%. Under NIR irradiation, IR780@Cu₉S₈ produced pronounced synergistic PTT-PDT effects against KYSE150 cells, causing a significant reduction of cell viability and marked suppression of cell proliferation, migration, and invasion. In the tumor-bearing mice, IR780@Cu₉S₈ and 808 nm laser irradiation exhibited strong synergistic PTT-PDT effects and significantly inhibited tumor growth with a good biocompatibility.</p><p><strong>Conclusions: </strong>The IR780@Cu₉S₈ composite nanoparticles achieve synergistic PTT-PDT antitumor activity in esophageal cancer cells which can be a promising strategy for combined therapy and targeted drug delivery for esophageal cancer.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"848-860"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776730","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":"[Visual prior-guided masked image modeling enhances chest X-ray diagnostic efficacy].","authors":"Jinger Wang, Yu Zhang","doi":"10.12122/j.issn.1673-4254.2026.04.23","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.23","url":null,"abstract":"<p><strong>Objectives: </strong>To develop a masked image modeling framework that integrates clinical visual priors to enhance semantic understanding and diagnostic performance on chest X-ray images.</p><p><strong>Methods: </strong>A novel framework VP-MIM was constructed by incorporating clinical visual priors into the MIM process. Eye-tracking data from radiologists were used to distinguish diagnostically relevant from irrelevant regions during the masking phase, enabling a controlled masking strategy. In the reconstruction phase, a pyramid attentive reconstruction module was developed to introduce multi-scale supervision, which was further refined by semantic-aware recalibrated gaze heatmaps to optimize feature learning.</p><p><strong>Results: </strong>Experiments conducted on the RSNA Pneumonia and ChestXray-14 public datasets showed that under linear evaluation with only 2616 pre-training samples, VP-MIM achieved an AUC of 86.83 on the RSNA Pneumonia single-label classification task and a mean AUC (mAUC) of 72.82 on the ChestXray-14 multi-label classification task. In full fine-tuning experiments, VP-MIM showed strong scalability when the amount of pre-training data increased, reaching an mAUC of 85.49 on ChestXray-14, which verified good scalability and excellent performance of this model in practical diagnostic tasks.</p><p><strong>Conclusions: </strong>VP-MIM alleviates the limitations of semantic loss and insufficient multi-scale modeling in medical imaging MIM to result in improved diagnostic performance of chest X-ray.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"946-955"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776707","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":"[Glutamine-induced autophagy exacerbates muscle atrophy in cachectic nude mice: a multi-omics analysis].","authors":"Ziyuan Li, Xiaoyu Su, Zhihan Tian, Xingliang Chao, Yong Wang, Dufang Ma","doi":"10.12122/j.issn.1673-4254.2026.04.10","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.10","url":null,"abstract":"<p><strong>Objectives: </strong>To clarify whether glutamine induces autophagy to promote skeletal muscle atrophy in cancer cachexia through integrated transcriptomic and metabolomic analyses.</p><p><strong>Methods: </strong>Twenty male BALB/c nude mice were randomized into control and model groups (<i>n</i>=10), and in the latter group cachexia was induced by subcutaneous implantation of CT-26 colon carcinoma cells. Tumor-free body mass and grip strength/body mass ratio of the mice were measured, myofiber transverse diameter was observed using HE staining, and muscle atrophy-related proteins (MuRF1 and atrogin-1) were detected. Transcriptomic and metabolomic analyses were used to identify the differentially expressed genes (DEGs) and differentially expressed metabolites (DEMs), respectively, and the metabolic pathways were mapped. Autophagosomes and gastrocnemius morphology were observed with transmission electron microscopy (TEM), and the autophagic markers (ULK1, LC3, and P62) and signaling pathway proteins (AMPK, FOXO3a, and mTOR) were assayed using Western blotting. The key findings were validated in C2C12 myoblasts treated with glutamine (Gln) and an AMPK inhibitor.</p><p><strong>Results: </strong>Compared with the control mice, the mice in the model group had significantly decreased tumor-free body mass, grip strength/body mass ratio and myofiber area with elevated atrogin-1 and MuRF1 expressions. The DEGs were mainly enriched in arginine/proline metabolism, AMPK, mTOR, autophagy and FOXO signaling pathways. Metabolomic analysis showed significantly increased glutamine and glutamate in the cachectic muscle. In the tumor-bearing mice, the number of autophagosomes increased significantly with blurred and fragmented myofibrils, upregulated AMPK/FOXO3a pathway proteins and ULK1, and downregulated mTOR pathway proteins and P62. In C2C12 myoblasts, treatment with glutamine obviously promoted autophagy, activated AMPK/FOXO3a signaling and inhibited the mTOR pathway, and these effects were strongly blocked by the AMPK inhibitor.</p><p><strong>Conclusions: </strong>Glutamine promotes autophagy through activation of the AMPK/FOXO3a signaling axis and suppression of the mTOR pathway, leading to skeletal muscle atrophy in cancer cachexia.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"816-824"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776683","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":"[Ursolic acid in <i>Huajie Xiaoliu</i> Formula inhibits colorectal cancer cell growth by inducing cuproptosis].","authors":"Chenghuan Jin, Zongchao Hong, Xueyun Duan, Heng Fan, Jingxing Yang, Jiamei Qin, Liyan Zou, Mengyuan Qin","doi":"10.12122/j.issn.1673-4254.2026.04.11","DOIUrl":"https://doi.org/10.12122/j.issn.1673-4254.2026.04.11","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the molecular mechanism by which <i>Huajie Xiaoliu</i> Formula (HJF) and its active component ursolic acid inhibit colorectal cancer (CRC) cell growth.</p><p><strong>Methods: </strong>Proteomics was used to analyze the effect of HJF on protein expression profile in CRC xenografts from tumor-bearing nude mice. Serum pharmacochemistry was used to identify the potential active components of HJF. Network pharmacology and molecular docking were employed to predict the interaction between ursolic acid and cuproptosis-related targets. Cellular assays including MTT, wound healing, colony formation, and Western blotting were used to validate the effects of ursolic acid on proliferation, migration, and cuproptosis-related indicators (FDX1, SLC31A1, DLAT, GSH, MDA, pyruvic acid, and Cu²⁺) in HCT-116 and LoVo cells.</p><p><strong>Results: </strong>HJF regulated 628 differentially expressed proteins in CRC, involving pathways related to inflammation, immunity, and metabolism. Ursolic acid was identified as a major blood component of HJF and exhibited a strong binding affinity with the key cuproptosis protein FDX1 (LiDock Score106.813). In HCT-116 and LoVo cells, ursolic acid significantly inhibited cell proliferation and migration, induced intracellular accumulation of Cu²⁺, MDA and pyruvic acid, reduced GSH levels, inhibited cellular DLAT expression, and up-regulated the expressions of FDX1 and SLC31A1.</p><p><strong>Conclusions: </strong>As one of the key active components in the HJF, ursolic acid inhibits CRC cell growth by inducing cuproptosis <i>via</i> targeting FDX1.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 4","pages":"825-837"},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147776675","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>Huangqin Qingre Chubi</i> Capsule inhibits JAK/STAT-driven synovial angiogenesis in rheumatoid arthritis by suppressing the LncRNA EBLN3P/miR-369-3p/NFIX axis].","authors":"Mengyu Sun, Yuan Wang, Feifei Liu","doi":"10.12122/j.issn.1673-4254.2026.03.21","DOIUrl":"10.12122/j.issn.1673-4254.2026.03.21","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the mechanism by which <i>Huangqin Qingre Chubi</i> Capsule (HQC) inhibits synovial angiogenesis mediated by the JAK/STAT pathway in rheumatoid arthritis (RA).</p><p><strong>Methods: </strong>An optimized co-culture model of RA-derived fibroblast-like synoviocytes (RA-FLS) and human umbilical vein endothelial cells (HUVECs) was treated with gradient concentrations of HQC-medicated serum with or without plasmid transfection for LncRNA EBLN3P overexpression. The inhibitory effects of HQC on pathological behaviors of RA-FLS were assessed using EdU assay, Transwell invasion assay, and scratch wound healing assay. Cellular secretions of pro-angiogenic factors (VEGF and FGF2) and matrix metalloproteinases (MMP2 and MMP9) were measured by ELISA. HUVEC tube formation capacity and expressions of the endothelial markers CD34 and CD105 were evaluated, and the expressions of molecules in the LncEBLN3P/miR-369-3p/NFIX axis and the JAK2/STAT3 pathway were detected using qRT-PCR and Western blotting.</p><p><strong>Results: </strong>The RA-FLS exhibited significantly enhanced proliferation, invasion, and migration with upregulated expressions of VEGF, FGF2, MMP2, and MMP9 and dysregulation of tthe LncEBLN3P/miR-369-3p/NFIX axis, as shown by decreased miR-369-3p and increased expressions of LncEBLN3P, NFIX, JAK2, STAT3, p-JAK2, and p-STAT3. Treatment with HQC-medicated serum effectively reversed these pathological changes, suppressed malignant phenotype of the cells, downregulated angiogenic and matrix-degrading factors, and inhibited the axis and pathway activity. In the LncRNA EBLN3P overexpression (OE-Lnc) model, HQC treatment less effectively reversed the pathological phenotype and pathway activation in the cells as compared to its effect in the non-overexpression setting.</p><p><strong>Conclusions: </strong>HQC inhibits pro-angiogenic function of RA-FLS likely by targeting the LncRNA EBLN3P/miR-369-3p/NFIX axis, thereby suppressing the downstream JAK/STAT signaling pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 3","pages":"675-685"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021347/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147521335","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":"[Formononetin downregulates P53/SAT1/ACSL4 pathway-mediated ferroptosis to improve hypoxic-ischemic brain injury in neonatal mice].","authors":"Tao Guo, Bolin Chen, Xiao Yang, Yanli Zhao, Xiaomin Li, Jiahao He, Jinsha Shi, Hanjun Zuo, Juanjuan Li","doi":"10.12122/j.issn.1673-4254.2026.03.14","DOIUrl":"10.12122/j.issn.1673-4254.2026.03.14","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the neuroprotective effects of formononetin (FMN) against hypoxic-ischemic brain damage (HIBD) in neonatal mice and the underlying mechanism.</p><p><strong>Methods: </strong>Twenty-four neonatal C57BL/6J mice were randomly divided (<i>n</i>=6) into sham-operated group, HIBD model group, HIBD+FMN-L (50 mg/kg) group, and HIBD+FMN-H (100 mg/kg) group. Mouse models of HIBD were established by left common carotid artery ligation followed by hypoxia (92% N₂, 8% O₂) for 40 min. FMN at the two doses was administered by intraperitoneal injection, and 3 days later, brain tissues from the cortical ischemic penumbra were collected for assessing expressions of ferroptosis-related proteins (P53, SAT1, and ACSL4) using Western blotting and immunofluorescence staining and for detecting the levels of Fe²⁺, superoxide, malondialdehyde (MDA), and glutathione (GSH). In cultured HT22 neurons with oxygen-glucose deprivation (OGD), the effects of 100 μmol/L FMN, 10 μmol/L Nutlin-3 (a P53 agonist), or their combination on expressions of ferroptosis proteins, intracellular Fe²⁺, reactive oxygen species (ROS), lipid peroxidation, GSH, mitochondrial membrane potential, and cell viability were evaluated.</p><p><strong>Results: </strong>In the neonatal mouse models of HIBD, FMN treatment significantly suppressed the protein expression of P53, SAT1, and ACSL4, reduced Fe²⁺, ROS, and MDA levels and increased GSH content in the cortical ischemic penumbra. In HT22 neurons with OGD, FMN obviously alleviated OGD-induced ferroptosis as shown by lowered expressions of the key ferroptosis proteins, reduced Fe²⁺ accumulation and lipid peroxidation, and significant increases of GSH levels, mitochondrial membrane potential, and cell viability. Mechanistic experiments showed that activation of P53 signaling by Nutlin-3 markedly reversed the protective effects of FMN.</p><p><strong>Conclusions: </strong>FMN produces neuro-protective effects against HIBD in neonatal mice by mitigating neuronal ferroptosis, primarily through downregulation of the P53/SAT1/ACSL4 signaling pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 3","pages":"604-614"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147521436","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":"[Identification of efferocytosis-related genes in osteoarthritis and prediction of traditional Chinese medicines based on bioinformatics and machine learning].","authors":"Kelin Xiang, Xiaoyu Zhang, Zhengpeng Li, Zhiwei Xu, Sujie Liu, Yuan Chai","doi":"10.12122/j.issn.1673-4254.2026.03.23","DOIUrl":"10.12122/j.issn.1673-4254.2026.03.23","url":null,"abstract":"<p><strong>Objectives: </strong>To screen key genes related to efferocytosis in osteoarthritis (OA) based on bioinformatics and machine learning methods, and explore their diagnostic value, immune microenvironment characteristics, and potential therapeutic targets of traditional Chinese medicines (TCM).</p><p><strong>Methods: </strong>OA-related datasets GSE55235, GSE55457, and GSE117999 were obtained from the GEO database. An efferocytosis-related gene set was retrieved from GeneCards. Differential expression analysis was performed to identify OA-related differentially expressed genes (DEGs) and their intersection with efferocytosis-related genes, followed by GO and KEGG enrichment analyses. Three machine learning algorithms (Random Forest, LASSO regression, and SVM) were used to screen feature genes, and their diagnostic efficacy was evaluated using ROC curves. qRT-PCR was used to validate the feature gene expressions in a rat OA model. Immune cell infiltration was analyzed using CIBERSORT, GSEA was used to explore the related pathways, and the Coremine database was utilized to predict TCMs associated with the feature genes.</p><p><strong>Results: </strong>A total of 959 OA-related DEGs were identified, including 15 efferocytosis-related genes, which were enriched in leukocyte migration, extracellular matrix, and inflammatory pathways. Machine learning identified 3 feature genes, namely UCP2, EGLN3, and IL1B, which showed good diagnostic performance in both the training (GSE55235) and validation sets (GSE55457 and GSE117999) and varying expression patterns in the mouse models. Immune infiltration analysis showed significant differences in resting mast cells, resting memory CD4⁺ T cells, and activated mast cells between OA patients and healthy controls. The feature genes were closely associated with the adipocytokine signaling pathway, sulfur metabolism, and spliceosome pathway. A total of 100 TCMs were predicted, which were primarily herbs for tonifying deficiency, clearing heat, and promoting blood circulation, such as Lycium barbarum, Epimedium brevicornu, Rehmannia glutinosa, Sophora flavescens, Ligusticum chuanxiong, and Achyranthes bidentata.</p><p><strong>Conclusions: </strong>Efferocytosis-related genes play important roles in OA pathogenesis. UCP2, EGLN3, and IL1B have diagnostic value for OA. The predicted TCMs may serve as potential agents for OA prevention and treatment.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 3","pages":"693-706"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147521450","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":"[Eurycomanone inhibits renal ischemia/reperfusion-induced mitochondrial dysfunction and inflammation in mice by binding to STAT3 to inhibit its phosphorylation].","authors":"Ze Liu, Zhangkun Mao, Da You, Junjie Wang, Yongmei He, Yiwen Yu, Zhiqiang Wen, Huilong Fang, Wenxia He","doi":"10.12122/j.issn.1673-4254.2026.03.11","DOIUrl":"10.12122/j.issn.1673-4254.2026.03.11","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the mechanism of eurycomanone (EN) for ameliorating ischemia/reperfusion (IR)-induced acute kidney injury (AKI) in mice.</p><p><strong>Methods: </strong>Twenty-four male C57BL/6J mice were randomly divided into 4 groups (<i>n</i>=6) for sham operation, IR modeling by bilateral renal pedicle clamping, or intraperitoneal injections of EN at 0.25 or 1.0 mg/kg for two days prior to surgery. Network pharmacology and molecular docking were used to identify the potential molecular targets and signaling pathways and evaluate the binding affinities. Renal function, histopathological changes, expression of tubular injury markers (KIM-1 and NGAL), phosphorylation levels of STAT3, PI3K, and JAK2, renal inflammation, mitochondrial biogenesis, and mitochondrial function of the mice were assessed. The interaction between EN and STAT3 was examined using surface plasmon resonance (SPR). Another 24 male C57BL/6J mice receiving sham operation, IR modeling, or EN or EN+ML115 (a STAT3 agonist) treatment prior to modeling (<i>n</i>=6) were used to validate the role of STAT3 in EN-mediated renal protection.</p><p><strong>Results: </strong>Both low- and high-dose EN significantly alleviated renal injury and improved renal function in mice with IR-induced AKI. The core targets of EN were associated with inflammation-related signaling pathways. EN treatment markedly reduced renal levels of IL-6, MCP-1, and TNF-αand decreased macrophage infiltration (F4/80-positive cells) in renal interstitial tissue of the mice. EN also significantly increased renal ATP content and mitochondrial DNA copy number (<i>P</i><0.05), and upregulated the expressions of PGC-1α, TFAM, and Nrf2 mRNAs and protein levels of PGC-1α and TOM20. Molecular docking identified STAT3 and PI3K as key molecular targets of EN. In mice with IR-induced AKI, EN significantly suppressed phosphorylation of STAT3 and PI3K in the renal tissues without affecting p-JAK2 levels. SPR analysis confirmed a direct and specific interaction between EN and STAT3. Notably, activation of STAT3 by ML115 significantly reversed the renoprotective effects of EN.</p><p><strong>Conclusions: </strong>EN mitigates IR-induced AKI in mice by directly binding to STAT3 to inhibit its phosphorylation, suppressing inflammation, and enhancing mitochondrial biogenesis and function, suggesting the potential of EN as a promising therapeutic candidate for IR-induced AKI.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 3","pages":"570-581"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147521471","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":"[Selenocystine inhibits colon cancer cell growth by promoting reactive oxygen species generation to trigger oxidative damage].","authors":"Qile Song, Yikai Miao, Xiaotong Feng, Yifan Wang, Wei Liu, Qi Wei, Xinru Yu, Wenwen Chen, Xiaoyan Fu","doi":"10.12122/j.issn.1673-4254.2026.03.07","DOIUrl":"10.12122/j.issn.1673-4254.2026.03.07","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the molecular mechanism by which selenocystine (SeC) inhibits colon cancer cell growth <i>in vitro</i>.</p><p><strong>Methods: </strong>Colon cancer cells (RKO, HCT-116, and LoVo) were cultured and treated with 5, 10, or 20 μmol/L SeC for 24 h and 48 h. MTT assay was used to detect the cell viability, and wound healing assay was used to examine changes in cell migration. Flow cytometry with PI staining was used to analyze cell cycle arrest and apoptosis. Fluorescence probes were employed to monitor reactive oxygen species (ROS) generation, mitochondrial morphology and membrane potential, and the changes in ferroptosis were evaluated by detecting malondialdehyde (MDA), glutathione (GSH) and ferrous ion (Fe²⁺) levels; Western blotting was used to detect the changes in protein expressions.</p><p><strong>Results: </strong>SeC at all the 3 doses significantly inhibited proliferation and migration of colon cancer cells, down-regulated the expression of cell cycle-related proteins CDK2 and CDK4 and activated the apoptotic proteins PARP and caspase-9. Western blotting showed that SeC decreased the expression of ferroptosis proteins FTH1 and xCT and increased the expression of DMT1. The levels of MDA and Fe²⁺ were increased and GSH level was decreased in SeC-treated cells. Fluorescence staining results showed that SeC treatment induced mitochondrial structure damages and promoted cellular ROS production. SeC treatment also increased phosphorylation of oxidative damage proteins and lowered the expression levels of NRF2 and HO-1 proteins. ROS scavenger significantly reversed the up-regulation of DMT1, PARP and p-H₂A.X protein induced by SeC in colon cancer cells.</p><p><strong>Conclusions: </strong>SeC induces apoptosis and ferroptosis of colon cancer cells by promoting ROS generation and initiating oxidative damage, suggesting the potential of SeC as a potential chemotherapeutic agent for colon cancer.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 3","pages":"532-540"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147521512","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 nomogram model for predicting MACE risk following primary percutaneous coronary intervention in STEMI patients: an exploratory study based on serum GSDMD].","authors":"Xinyi Hu, Weijian Wang, Hui Li, Zongzheng Chen, Xin Zhou, Junfei Yuan, Liang Chen","doi":"10.12122/j.issn.1673-4254.2026.03.09","DOIUrl":"10.12122/j.issn.1673-4254.2026.03.09","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the value of serum gasdermin D (GSDMD) level for predicting 30-day major adverse cardiovascular events (MACE) in patients following primary percutaneous coronary intervention (PPCI) for acute ST-segment elevation myocardial infarction (STEMI) and construct a predictive nomogram.</p><p><strong>Methods: </strong>A total of 100 STEMI patients undergoing PPCI were prospectively enrolled. Serum GSDMD levels of the patients were measured by ELISA before and on the second morning after PPCI and compared using Wilcoxon signed-rank test. The patients were divided into high-GSDMD and low-GSDMD groups based on the optimal cut-off value of postoperative GSDMD levels determined by the Youden index. During the 30-day follow-up, the patients were categorized into MACE group (<i>n</i>=26) and non-MACE group (<i>n</i>=74). The key predictors were selected using univariable and LASSO regression, followed by multivariable logistic regression to identify the independent risk factors. A nomogram was constructed and evaluated by ROC curve analysis, Bootstrap internal validation, Hosmer-Lemeshow test, calibration plots and decision curve analysis (DCA).</p><p><strong>Results: </strong>Post-PPCI serum GSDMD levels were significantly elevated relative to the pre-PPCI levels (<i>Z</i>=-4.848, <i>P</i><0.001). The incidence of 30-day MACE was significantly higher in the high GSDMD group (<i>P</i>=0.01). Post-PPCI GSDMD level was identified as an independent risk factor for short-term MACE. The final nomogram incorporated Killip classification, number of stents, albumin, and post-PPCI GSDMD and demonstrated good predictive performance with an AUC of 0.847 (<i>P</i><0.001, 95% <i>CI</i>: 0.759-0.936), a sensitivity of 84.6% and a specificity of 79.7%. All the validation analyses confirmed good predictive efficacy and clinical utility of the model.</p><p><strong>Conclusions: </strong>Elevated post-PPCI serum GSDMD level is an independent risk factor for 30-day MACE in STEMI patients. The nomogram model based on this biomarker provides a reliable tool for short-term risk stratification of these patients.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 3","pages":"550-558"},"PeriodicalIF":0.0,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147521513","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}