南方医科大学学报杂志最新文献

{"title":"[Perioperative outcomes and anesthetic management of pregnancy termination in patients with pulmonary hypertension].","authors":"Liting Yang, Feng Zhong, Jingyi Zhang, Yingxian Ye, Wenjin Ji, Haihua Shu, Yanli Liu, Jiexian Liang","doi":"10.12122/j.issn.1673-4254.2026.08.12","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.12","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate outcomes of pregnancy termination in women with pulmonary hypertension (PH) and the correlations of anesthetic management strategies and intraoperative blood pressure variability with postoperative adverse events.</p><p><strong>Methods: </strong>Sixty-two women underwent termination of pregnancy complicated by PH from June, 2019 to December, 2024 in Guangdong Provincial People's Hospital, including 24 women with mild-to-moderate PH and 38 with severe PH. Perioperative parameters and clinical outcomes of the patients were compared between the two groups.</p><p><strong>Results: </strong>The most common subtype of PH in these women was pulmonary arterial hypertension (82.3%), caused primarily by congenital heart diseases (most frequently atrial or ventricular septal defects). The majority of the women underwent pregnancy termination by dilation and curettage (<i>P</i>=0.02) under general anesthesia (<i>P</i>=0.002). A total of 5 postoperative adverse events were recorded, including PH crisis (3 cases), arrhythmia requiring intervention (1 case), and pulmonary embolism (1 case). After multivariate adjustment, the severity of PH was significantly correlated with both postoperative ICU admission and prolonged postoperative length of stay (<i>P</i><0.05). Among the patients undergoing dilation and curettage, the incidence of postoperative adverse events was significantly higher in patients receiving intrathecal anesthesia (<i>P</i>=0.014). A high blood pressure variability during surgery was correlated with a high rate of postoperative adverse events (<i>P</i><0.05), which was significantly lower in patients with a blood pressure variability below the third tertile (OR=10.25, 95% <i>CI</i>=1.06-98.84, <i>P</i>=0.034).</p><p><strong>Conclusions: </strong>Postoperative recovery following pregnancy termination is associated with the severity of PH. Anesthetic methods for pregnancy termination should be individualized. Patients with a high intraoperative blood pressure variability have an increased risk of postoperative adverse events, and inhaled nitric oxide therapy is effective for reducing pulmonary arterial pressure during surgery.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1850-1860"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707139","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":"[Prognostic value of palmitoyl-protein thioesterase-1 in gastric cancer and its regulatory role in tumor cell lipid metabolism].","authors":"Bingyi Huang, Yujie Gao, Jingyi Xie, Chen Yan, Mengru Gu, Zhizhi Zhang, Jintao Guo, Song Liu, Ziliang Wang, Yuping Yang, Lugen Zuo, Deli Chen","doi":"10.12122/j.issn.1673-4254.2026.08.19","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.19","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate palmitoyl-protein thioesterase-1 (PPT1) expression in gastric cancer (GC), its prognostic significance, and its regulatory role in tumor cell lipid metabolism.</p><p><strong>Methods: </strong>PPT1 expression was analyzed using TCGA-STAD data and immunohistochemistry of clinical samples. In a retrospective cohort of 136 GC patients undergoing radical resection, the association between PPT1 and 5-year survival was evaluated using Kaplan-Meier and Cox regression analyses, and a nomogram was constructed and validated by ROC analysis. GO and REACTOME enrichment analyses were conducted to identify the pathways involved. In cultured GC cell lines with PPT1 knockdown or overexpression, the changes in cell proliferation, migration and invasion were assessed using CCK-8 and Transwell assays. Oil Red O staining, Western blotting and U0126 rescue experiments were performed to explore the role of PPT1-mediated ERK signaling in tumor cell lipid metabolism.</p><p><strong>Results: </strong>PPT1 protein, localized in the cytoplasm, was significantly upregulated in GC tissues compared with adjacent normal tissues. High PPT1 expression was closely correlated with elevated serum CEA and CA19-9 levels and advanced T and N stages (<i>P</i><0.05), and was an independent risk factor for reduced 5-year postoperative survival. The nomogram incorporating PPT1 showed good predictive accuracy (C-index=0.812) with an AUC of 0.837. In cultured GC cells, PPT1 knockdown significantly suppressed while PPT1 overexpression promoted cell proliferation, migration and invasion. PPT1 overexpression induced abnormal intracellular lipid accumulation in GC cells and significantly upregulated the expressions of the key lipogenic proteins SREBP 1 and FASN, and this pro-lipogenic effect and subsequent ERK signaling activation were effectively reversed by U0126.</p><p><strong>Conclusions: </strong>PPT1 is overexpressed in GC tissues and predicts poor prognosis. PPT1 overexpression promotes GC progression by activating the ERK signaling pathway and thereby modulating lipid metabolism, suggesting its potential as a novel prognostic biomarker and a therapeutic target for GC.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1915-1925"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707164","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":"[Everolimus inhibits malignant phenotype of erdafitinib-resistant bladder cancer cells through the p70S6K/PI3K/MAPK signaling pathway].","authors":"Haosong Wu, Yi Jiang, Xiaolin Zhang, Sheng Wang","doi":"10.12122/j.issn.1673-4254.2026.08.14","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.14","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the regulatory effect of everolimus on biological behaviors of rdafitinib-resistant bladder cancer cells and the underlying mechanism.</p><p><strong>Methods: </strong>An erdafitinib-resistant RT-112-RS cell model was established by continuous induction of RT-112 cells with erdafitinib at the optimized concentration (5 μmol/L) for 16 weeks. The resistant cells were treated with PDGF-BB alone or in combination with 0.01, 0.1, or 1 μmol/L everolimus, and the cytotoxicity (IC₅₀) of everolimus was determined with CCK-8 assay. The changes in cell migration and invasion were evaluated using scratch wound healing assay and Transwell assays. The expressions of the genes of interest in the cells treated with everolimus (0.001- 1 μmol/L) were detected using RT-qPCR, and cell apoptosis was analyzed with flow cytometry. Western blotting was performed to assess phosphorylation levels of the key proteins in the mTORC1/p70S6K, PI3K/Akt, and Raf1/MEK/ERK pathways.</p><p><strong>Results: </strong>Everolimus within the concentration range of 0.001-0.1 μmol/L dose-dependently inhibited RT-112-RS cell proliferation. RT-112-RS cells showed significantly enhanced migration and invasion compared with their parental RT-112 cells. Treatment with 1 μmol/L everolimus significantly suppressed p70S6K phosphorylation but did not result in an enhanced inhibition of cell proliferation effect. Everolimus at 1 μmol/L significantly activated the Raf1/MEK/ERK pathway without affecting PI3K/Akt (Thr308) or mTORC2/Akt (Ser473) phosphorylation. Treatment of the cells with the MEK inhibitor U-0126 obviously reversed everolimus-induced ERK1/2 activation, while the PI3K inhibitor LY294002 only partially reduced ERK1/2 activation in everolimus-treated cells.</p><p><strong>Conclusions: </strong>Everolimus inhibits RT-112-RS cell proliferation by suppressing p70S6K activity, and at high concentrations, everolimus can result in activation of the PI3K-Raf1/MEK/ERK pathway possibly by relieving negative feedback inhibition to partially offset its inhibitory effect on cell proliferation.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1870-1877"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706722","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":"[Isolation, purification and immunomodulatory activity of polysaccharide from <i>Lonicera caerulea</i> L. var. <i>edulis</i> Turcz. ex Herder].","authors":"Yangjia Huang, Xudong Zhang, Qianru Xiang, Hanquan Guo, Shuang Zheng, Yuting Hao, Wenzhen Liao","doi":"10.12122/j.issn.1673-4254.2026.08.08","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.08","url":null,"abstract":"<p><strong>Objectives: </strong>To isolate a novel polysaccharide (THP-2) from <i>Lonicera caerulea</i> L.var. <i>edulis</i> Turcz. ex Herder (<i>L. caerulea</i>) and evaluate its immunomodulatory activity.</p><p><strong>Methods: </strong>Ultrasonic-assisted water extraction and alcohol precipitation and gel column chromatography were used to separate and purify polysaccharides from <i>L.caerulea</i>. The relative molecular mass, purity and chemical structure of THP-2 were analyzed by gel permeation chromatography, ion chromatography, periodate oxidation and smith degradation, infrared spectroscopy, nuclear magnetic resonance spectroscopy and Congo red experiment. DC2.4 cells and Raw264.7 cells were used to evaluate the immunomodulatory activity of THP-2.</p><p><strong>Results: </strong>A new polysaccharide component THP-2 was isolated and purified from <i>L.caerulea</i>, and its chemical composition and structural characteristics were significantly different from those of <i>L.caerulea</i> polysaccharide reported previously. The average relative molecular mass of THP-2 was 123 090, and its monosaccharide components included sugar, galactose, glucose, mannose, xylose, glucuronic acid and galacturonic acid with a molar ratio of 27.84:52.28:8.47:6.05:2.75:0.90:0.88:0.83. Glycosidic bond analysis showed that THP-2 was mainly composed of (1→5), (1→3), (1→4), (1→6), (1→3,4), (1→6,4) and other glycosidic bonds. THP-2 could activate expressions of costimulatory molecules CD80, CD86, CD40 and MHC-II and promote IL-1β, IL-6 and TNF-α secretion in DC2.4 cells, up-regulate CD80, CD86 and CD40 expressions and enhance the expressions of IL-1β, IL-6 and TNF-α in Raw264.7 cells. THP-2 also promoted iNOS expression, increased NO secretion, and up-regulated p-p65 and p-IκB expressions in both cells, and increased p-Akt protein content in DC2.4 cells.</p><p><strong>Conclusions: </strong>The new polysaccharide component THP-2 isolated from <i>L.caerulea</i> is capable of promoting maturation and differentiation of DC2.4 cells by activating the NF‑κB signaling pathway and PI3K/Akt pathway and promoting the differentiation of Raw264.7 cells into M1 macrophages through the NF-κB pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1799-1813"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706963","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":"[Prediction and verification of therapeutic drugs for triple-negative breast cancer using a knowledge graph-based drug repurposing model].","authors":"Diheng Wu, Zhanfa Xu, Yi Li, Mingxu Zhang, Jiaze Lin, Yijun Lü, Daogang Guan, Genggeng Qin","doi":"10.12122/j.issn.1673-4254.2026.08.22","DOIUrl":"10.12122/j.issn.1673-4254.2026.08.22","url":null,"abstract":"<p><strong>Objectives: </strong>To construct a knowledge graph-based drug repurposing model for predicting potential therapeutic drugs for triple-negative breast cancer (TNBC).</p><p><strong>Methods: </strong>Drug-target interaction (DTI) affinity data were collected from the BindingDB database and filtered (including data of Kd, Ki, EC₅₀ and IC₅₀). The proposed KGNN model integrates graph convolutional network (GCN)‑extracted drug molecular graph features, ProtBERT-pretrained protein sequence representations, and STRING-derived protein-protein interaction (PPI) knowledge graphs. Multi-head attention mechanisms and gated fusion modules were used to model interaction dependencies. Model performance was evaluated using mean squared error (MSE), Pearson correlation coefficient (PCC), and concordance index (CI). Ablation studies were performed to assess module contributions, and cold-start experiments were conducted to test generalization ability of the model. Using data from TCGA, 1340 TNBC-associated pathogenic genes were screened by bioinformatics analyses and mapped to targets using UniProt. KGNN was applied to predict the candidate drugs, which were validated through molecular docking and molecular dynamics simulations.</p><p><strong>Results: </strong>In the DTI affinity prediction task, KGNN outperformed the benchmark models including KronRLS, SimBoost, DeepDTA, FusionDTA, and GraphDTA (MSE=3.2697, PCC=0.8037, and CI=0.7862). Ablation studies confirmed the critical roles of the modules for enhancing model performance (multi-head attention increased MSE by 5.60%; PPI fusion increased MSE by 10.82%). In cold-start scenarios, KGNN maintained superior performance over the comparators in unseen drug/target settings, demonstrating robust generalization. The TNBC candidate drug predictions well aligned with docking affinities and dynamics simulations (Pearson correlation coefficient>0.85), while attention visualization highlighted the efficacy hotspots.</p><p><strong>Conclusions: </strong>The KGNN model can effectively predict drug-target interactions to facilitate drug repurposing and the design of multi-target drugs while reducing the screening space and experimental validation costs.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 8","pages":"1947-1955"},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13458599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707171","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":"[Lonicera japonica attenuates oxidative stress and improves post-ischemic heart failure in mice <i>via</i> the STAT3/PGC-1α axis].","authors":"Miao Li, Guiying Yu, Jincheng Wang, Kang Xie, Yulin Ouyang, Neng Wang, Ruijia Wen, Wei Wang, Chun Li","doi":"10.12122/j.issn.1673-4254.2026.07.10","DOIUrl":"10.12122/j.issn.1673-4254.2026.07.10","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the mechanism by which freeze-dried water extract of Lonicera japonica alleviates oxidative stress and improves post-ischemic heart failure in mice.</p><p><strong>Methods: </strong>Bioinformatics analyses were carried out to identify the active constituents in Lonicera japonica, their target genes, and their enrichment pathways. Mouse models of ischemic heart failure established by left anterior descending (LAD) artery ligation were treated with different doses of freeze-dried water extract of Lonicera japonica, and the changes in cardiac function, myocardial pathology and expressions of the STAT3/PGC-1α axis were examined. In cultured H9C2 cells with oxygen-glucose deprivation (OGD), the effects of Lonicera japonica extract on cell viability, reactive oxygen species (ROS) production and apoptosis were evaluated, and its regulatory effects on STAT3 and PGC-1α expression were assessed using Western blotting and immunofluorescence staining; mass spectrometry was employed to analyze the tissue-penetrating components of Lonicera japonica extract, and the binding capacities of its major constituents to STAT3 and PGC-1α were simulated with molecular docking studies.</p><p><strong>Results: </strong>In mice with ischemic heart failure, treatment with Lonicera japonica extract significantly improved the cardiac function and alleviated myocardial hypertrophy, inflammatory responses and collagen deposition. The treatment also restored cell viability of H9C2 cells with OGD and reduced cellular ROS production and cell apoptosis. Lonicera japonica extract significantly inhibited STAT3 activation and upregulated PGC-1α expression in H9C2 cells with OGD, and this effect was effectively attenuated by application of the STAT3 agonist Colivelin. Molecular docking results suggested that among the components of Lonicera japonica extract capable of entering the myocardial tissues, lonicerin, chlorogenic acid and 1,5-dicaffeoylquinic acid had strong binding affinity with STAT3 and PGC-1α.</p><p><strong>Conclusions: </strong>Lonicera japonica extract alleviates myocardial oxidative stress and improves heart failure in mice via the STAT3/PGC-1α axis, suggesting the value of Lonicera japonica in the treatment of heart failure.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 7","pages":"1563-1575"},"PeriodicalIF":0.0,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13391600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562559","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":"[Buffering effect of intensive lipid lowering on mortality risk in type 2 diabetic patients with chronic kidney disease and challenging glycemic management: a cohort study based on dual metabolic trajectories].","authors":"Xiaolong Wang, Jian Yang, Shuang Liang, Zheyi Dong","doi":"10.12122/j.issn.1673-4254.2026.07.17","DOIUrl":"10.12122/j.issn.1673-4254.2026.07.17","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the longitudinal synergistic evolution of low-density lipoprotein cholesterol (LDL-C) and glycated hemoglobin (HbA1c) in patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD), and analyze the interaction effects and risk-modifying effect of dual metabolic trajectories on all-cause mortality.</p><p><strong>Methods: </strong>This study included 7991 patients with T2DM and CKD based on the Tianjin medical insurance data platform. Group-based trajectory modeling (GBTM) was employed to identify longitudinal trajectory patterns of LDL-C and HbA1c, and dual metabolic trajectory groups were constructed to evaluate their synergistic effects. LASSO regression was applied for feature selection. Multivariable Cox proportional hazards regression with a dual-reference group strategy was utilized to systematically quantify the combined risks of dual trajectories and specifically assess the risk modification value of intensive lipid lowering across different glycemic backgrounds.</p><p><strong>Results: </strong>During a median follow-up of 5.10 (3.15-7.52) years, 405 deaths (5.1%) were recorded. Three LDL-C trajectories (Intensive Control, Standard Control, and High-Regression) and 3 HbA1c trajectories (Well-Controlled, Moderate Improvement, and Poorly Controlled) were identified. Dual metabolic disturbances demonstrated a significant dose-response gradient, with the \"Lipid-Poor/Glucose-Poor\" group exhibiting the highest mortality risk (HR=5.550, 95% <i>CI</i>: 3.322-9.274, <i>P</i><0.001), far exceeding the additive risk of single-indicator abnormalities. Even with well-controlled HbA1c, the high-regression LDL-C trajectory independently increased mortality risk (HR=2.015, <i>P</i>=0.039). Conversely, under intensive LDL-C control, the excess risk associated with poorly controlled HbA1c was no longer significant (<i>P</i>=0.480). Interaction analysis confirmed that for patients with poorly controlled HbA1c, intensifying LDL-C to a deep control level (<1.8 mmol/L) had a significant buffering protective effect compared to standard lipid lowering, reducing the mortality risk by 51% (HR=0.49, 95% <i>CI</i>: 0.26-0.92, <i>P</i>=0.026); in contrast, de-escalating from intensive to standard control increased the risk by 99% (HR=1.99, 95% <i>CI</i>: 1.07-3.69, <i>P</i>=0.029).</p><p><strong>Conclusions: </strong>This study reveals for the first time the longitudinal synergistic evolution of glucose and lipid metabolic trajectories in patients with T2DM and CKD and their superimposed impact on prognosis. Intensive lipid lowering (LDL-C<1.8 mmol/L) confers a significant protective effect in patients with difficulty in glycemic management and serves as an effective compensatory strategy to improve patient prognosis.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 7","pages":"1634-1647"},"PeriodicalIF":0.0,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13391599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562519","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>Miao</i> medicine <i>Sidaxue</i> regulates macrophage polarization and alleviates synovial inflammation in collagen-induced arthritis rats by inhibiting HIF-1α/PDK1-mediated glycolytic reprogramming].","authors":"Wanting Shen, Yizhe Chen, Xinyu Fu, Jiatao Yuan, Jun Zhou, Li Huang, Ning Wu","doi":"10.12122/j.issn.1673-4254.2026.09.08","DOIUrl":"10.12122/j.issn.1673-4254.2026.09.08","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the mechanism of <i>Miao</i> medicine prescription <i>Sidaxue</i> (SX) for inhibiting glycolysis in the synovial tissue and promoting macrophage polarization in rats with collagen-induced arthritis (CIA).</p><p><strong>Methods: </strong>Thirty-two SD rats were randomized into normal control group, CIA model group, tripterygium glycosides (40 mg/kg; positive control) treatment group, and SX (40 g/kg) treatment group (<i>n=</i>8). Except for those in the normal control group, all the rats were subjected to CIA modeling and treated with saline, tripterygium glycosides or SX by gavage for 21 consecutive days. Paw swelling, arthritis index, synovial pathology, inflammatory factors, glycolysis-related indicators and gene expressions were detected. UHPLC-MS was used to screen the components of SX in the blood of SX-treated rats. The target genes of the active components of SX and rheumatoid arthritis (RA) were predicted using bioinformatics analysis, and the hub genes were identified using machine learning algorithms. The binding sites between HIF-1α and PDK1 were predicted using AlphaFold3, and the interactions between SX components and their targets were simulated using molecular docking.</p><p><strong>Results: </strong>SX treatment significantly alleviated joint swelling, lowered arthritis scores, improved synovial lesions, and reduced serum levels of TNF-α, IL-1β and IL-6 in CIA rats, resulting in also inhibition of macrophage polarization and down-regulation of HIF-1α, PDK1 and HK2 expressions in the synovial tissues. Twenty-nine components of SX were detected in the blood of SX-treated rats, and 9 key target genes were identified. AlphaFold3 predicted a strong interaction between HIF-1α and PDK1, and their virtual knockout was shown to disturb the inflammatory pathways in the macrophages. Molecular docking studies suggested stable docking between the active components of SX and their key targets.</p><p><strong>Conclusions: </strong>SX alleviates joint inflammation in CIA rats by inhibiting the HIF-1α/PDK1 signaling pathway, correcting glycolytic reprogramming, and promoting M2 polarization of macrophages.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 9","pages":"2078-2090"},"PeriodicalIF":0.0,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081704","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":"[Insights into the occurrence and heterogeneity of gastric cancer from the perspective of clinical data integration].","authors":"Yafang Huang, Simiao Yang, Xia Ding, Fuhao Chu, Runhua Chen","doi":"10.12122/j.issn.1673-4254.2026.09.25","DOIUrl":"10.12122/j.issn.1673-4254.2026.09.25","url":null,"abstract":"<p><p>From the perspective of clinical data integration, the authors systematically review recent advances in gastric cancer researches that integrate multi-omics technologies with clinical data. Gastric cancer is characterized by high incidence, high mortality, and significant heterogeneity, and this review analyzes the molecular classification system of gastric cancer and its driver genes by integrating multi-omics information-including genomics, transcriptomics, and proteomics-with clinical data, and further explores the mechanisms of interaction between cancer cells and stromal cells in the tumor microenvironment. On this basis, this review summarizes the clinical and molecular correlation patterns of different gastric cancer subtypes and constructs a comprehensive research framework that integrates clinical data, multi-omics networks, and the tumor microenvironment, thereby linking the mechanisms that drive the entire course of cancer progression from precancerous lesions to tumor advancement. This framework provides systematic theoretical support and a translational pathway for early prevention, screening, and precision diagnosis and treatment of gastric cancer, and contributes to the advancement of precision medicine in gastric cancer management.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 9","pages":"2276-2284"},"PeriodicalIF":0.0,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081269","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":"[Activation of the CaMKKβ/AMPK/HIF-1α signaling pathway promotes angiogenesis in endometriosis by regulating mitophagy].","authors":"Yuanhuan Chen, Bin Yue, Quansheng Wu, Haiyan Mao, Xiujia Ji, Cuijun Chu, Lin Chen, Yuzhi Zhang, Bingxia Li, Xiaohua Zhang, Peng Feng","doi":"10.12122/j.issn.1673-4254.2026.09.05","DOIUrl":"10.12122/j.issn.1673-4254.2026.09.05","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate whether the CaMKKβ/AMPK/HIF-1α signaling pathway participates in angiogenesis in endometriosis by regulating mitophagy.</p><p><strong>Methods: </strong>Human endometrial stromal cells (hEM15A) isolated from endometriosis patients and normal endometrial stromal cells (HESCs) from non-endometriosis women were tested for proliferation, invasion, migration and tube formation abilities using CCK-8 assay, scratch assay and in vitro angiogenesis test. The protein and mRNA expression levels of CaMKKβ, AMPK, HIF-1α, BNIP3, LC3, VEGF and CD31 in the cells were detected by Western blotting and qPCR. MitoTracker Green, MitoSOX Red fluorescent probes and immunofluorescence staining were used to observe mitochondrial morphology, mtROS level and BNIP3/LC3 co-localization. CaMKKβ agonists and inhibitors were used to verify the function of the CaMKKβ/AMPK/HIF-1α pathway.</p><p><strong>Results: </strong>Compared with HESCs, hEM15A cells showed stronger proliferation, invasion, migration and angiogenesis abilities with significantly up-regulated expressions of CaMKKβ, AMPK, HIF-1α, BNIP3, LC3, VEGF and CD31. hEM15A cells showed increased number of mitochondria with intact structure, but the localization signals of BNIP3 and LC3 and mtROS level increased significantly. Mechanistically, inhibition of CaMKKβ significantly reduced expressions of AMPK, BNIP3, LC3, HIF-1α, VEGF and CD31, while activation of CaMKKβ increased expressions these proteins, down-regulated mitochondrial autophagy and inhibited angiogenesis.</p><p><strong>Conclusions: </strong>CaMKKβ/AMPK is abnormally activated in endometriosis to result in excessive accumulation of HIF-1α, which in turn increases the expression of its downstream target gene BNIP3, thus promoting mitophagy to trigger abnormal angiogenesis, which can be inhibited by inhibiting abnormal activation of CaMKKβ.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 9","pages":"2046-2055"},"PeriodicalIF":0.0,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624976/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081674","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}