南方医科大学学报杂志最新文献

{"title":"[<i>Qingshen</i> Granules alleviate renal fibrosis in mice with unilateral ureteral obstruction by regulating Akt3-mediated M1 macrophage polarization].","authors":"Weili Wang, Yilin Gao, Xin Hong, Yizhen Chen, Meng Cheng, Lei Zhang, Rong Dai, Yiping Wang","doi":"10.12122/j.issn.1673-4254.2026.06.02","DOIUrl":"10.12122/j.issn.1673-4254.2026.06.02","url":null,"abstract":"<p><strong>Objectives: </strong>To clarify whether <i>Qingshen</i> Granules (QSG) inhibits renal fibrosis by regulating Akt3-mediated macrophage polarization.</p><p><strong>Methods: </strong>Adult C57BL/6 mice were randomized into Sham group, unilateral ureteral obstruction (UUO) model group, and UUO with QSG treatment group (<i>n</i>=6) for treatment with daily gavage of distilled water or QSG (4.0 g/kg) as indicated for 2 weeks. In AAV9 experiments, the mice received intrarenal injections of AAV9-shRNA(Akt3)-GFP for Akt3 knockdown or AAV9-shRNA-GFP (negative control) 2 weeks before sham operation or UUO modeling. After the treatments, the mice were examined for renal fibrosis, renal function, and macrophage polarization using HE staining, Masson staining, ELISA, Western blotting, RT-qPCR, immunohistochemistry, immunofluorescence staining, and flow cytometry. In the cell experiment, TGF‑β1-induced HK-2 cells were co-cultured with THP-1-derived macrophages, and the effects of QSG-medicated rat serum on cell viability, proliferation, and macrophage polarization were evaluated using CCK-8 and EdU assays, Western blotting and flow cytometry.</p><p><strong>Results: </strong>Compared with the sham-operated mice, the UUO mice showed impaired renal function, renal tubular injury, collagen deposition, upregulated expressions of IL-6 and TNF-α mRNA and α-SMA protein, and downregulated E-cad protein expression, which were significantly improved by QSG treatment. In AAV9 experiments, the UUO mice with control virus injection showed obvious renal fibrosis and increased M1 macrophages, while AAV9-shRNA(Akt3)‑GFP injection significantly alleviated renal fibrosis and inhibited M1 macrophage polarization without affecting M2 macrophages. In the co-cultured cells, treatment with QSG-medicated serum significantly reversed TGF-β1-induced reduction of HK-2 cell viability and proliferation, upregulated Akt3 and α‑SMA expressions, downregulated E-cad expression, and inhibited M0-to-M1 polarization of THP-1 cells induced by TGF‑β1-treated HK-2 cells.</p><p><strong>Conclusions: </strong>QSG alleviates renal fibrosis in UUO mice by inhibiting Akt3-mediated M1 macrophage polarization.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 6","pages":"1216-1227"},"PeriodicalIF":0.0,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13294742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318212","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":"[ZEB2 promotes glioblastoma progression by reprogramming lipid metabolism through the CYLD/FASN axis].","authors":"Zhenlin Chen, Peng Chai, Yangqi Mao, Ranxin Liu, Ye Song","doi":"10.12122/j.issn.1673-4254.2026.06.09","DOIUrl":"10.12122/j.issn.1673-4254.2026.06.09","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the role of ZEB2 in lipid metabolic reprogramming of glioblastoma and its mechanism for promoting glioblastoma progression.</p><p><strong>Methods: </strong>Mouse models bearing orthotopic intracranial xenografts derived from LN-229 and GBM007 cells with stable ZEB2 knockdown were used to assess tumor growth and mouse survival.. Lipid droplet accumulation, lipid composition, and membrane fluidity in the cells with ZEB2 knockdown were examined using Nile Red staining, transmission electron microscopy, untargeted lipidomics, and fluorescence recovery after photobleaching (FRAP). The candidate mediators were screened by integrating RNA sequencing, fatty acid synthase (FASN) immunoprecipitation-mass spectrometry, and BioGRID interaction data. Promoter luciferase assays, ChIP-qPCR, promoter mutagenesis, co-immunoprecipitation, protein degradation pathway inhibition, and ubiquitination assays were performed to investigate the regulatory role of the ZEB2-CYLD-FASN axis.</p><p><strong>Results: </strong>ZEB2 knockdown significantly suppressed intracranial glioblastoma growth and prolonged mouse survival. Glioblastoma cells with ZEB2 silencing showed reduced lipid droplet accumulation, decreased saturated fatty acid-associated storage lipids, increased phospholipid species containing polyunsaturated fatty acyl chains, and enhanced membrane fluidity. Mechanistically, ZEB2 knockdown reduced FASN protein abundance, whereas FASN restoration reversed lipid droplet reduction induced by ZEB2 silencing. Multi-omics screening identified CYLD as a key intermediate. ZEB2 was capable of directly binding to and activating the CYLD promoter. CYLD knockdown decreased FASN protein levels, whereas CYLD restoration recovered FASN abundance and lipid droplet formation. CYLD was co-localized and interacted with FASN. MG132 partially restored FASN abundance under ZEB2 knockdown, and CYLD overexpression reduced FASN ubiquitination.</p><p><strong>Conclusions: </strong>ZEB2 promotes glioblastoma lipid metabolic reprogramming and tumor progression by transcriptionally activating CYLD, which maintains FASN protein stability at least in part through ubiquitination-associated regulation.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 6","pages":"1290-1300"},"PeriodicalIF":0.0,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13294753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318115","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":"[Lactate induces gastric mucosal injury by promoting M1 polarization of macrophages <i>via</i> the cardio-gastric axis].","authors":"Yunheng Yang, Yaqing Jia, Gaosheng Yin, Shuangxiu Li, Ping Yang","doi":"10.12122/j.issn.1673-4254.2026.06.07","DOIUrl":"10.12122/j.issn.1673-4254.2026.06.07","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the role of lactate in myocardial ischemia-reperfusion (MIR)-induced gastric mucosal injury.</p><p><strong>Methods: </strong>Thirty C57BL/6J mice were randomized into sham-operated group, MIR (45 min ischemia and 2 h reperfusion) group, and MIR+LDHAI group, and gastric mucosal injury was assessed using macroscopic scoring and HE staining; serum lactate and cTnT levels were measured using ELISA. Metabolomics analysis was conducted to identify the differential serum metabolites between the sham-operated and MIR mice. In the cell experiment, human gastric mucosal cells (GES-1) were indirectly co-cultured with THP-1 cell-derived macrophages polarized to the M1 phenotype by lactate and/or lipopolysaccharide (LPS) stimulation. In both the gastric mucosa tissues of the mice and the co-cultured GES-1 cells, the protein expression levels of CD68, iNOS, Arg-1, COX-1, and COX-2 were detected using Western blotting and immunofluo-rescence staining.</p><p><strong>Results: </strong>Compared to sham operation, MIR induced concurrent injury in both the heart and stomach of the mice and caused elevation of iNOS protein levels and reduction of Arg-1 protein expression in the gastric mucosa, where increased overlapping fluorescent areas were detected after MIR using fluorescent double-labeling for CD68 and iNOS. Serum metabolomics analysis revealed a significant increase in circulating lactate levels after MIR. In GES-1 cells, indirect co-culture with M1 macrophages induced obvious cell injury, decreased COX-1 expression, and increased cellular COX-2 protein expression. Western blotting and immunofluorescence staining confirmed that 15 mmol/L lactate significantly increased iNOS and decreased Arg-1 expression in THP-1-derived macrophages. Indirect co-culture of GES-1 cells with M1 macrophages induced by lactate or LPS resulted in obvious GES-1 cell injury. In the mouse models of MIR, inhibition of lactic acid production effectively alleviated MIR-induced gastric mucosal injury.</p><p><strong>Conclusions: </strong>Lactate-induced M1 macrophage polarization mediates MIR-related gastric mucosal injury in mice via the heart-gastric axis, an effect reversible by LDHA inhibition.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 6","pages":"1267-1277"},"PeriodicalIF":0.0,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13294748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318315","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":"[1,3-dicaffeoylquinic acid mitigates dextran sulfate sodium-induced colitis in mice by alleviating oxidative stress <i>via</i> inhibiting the PI3K/Akt pathway].","authors":"Lin Yin, Yu Zhang, Keni Zhang, Tong Qiao, Longtao Zhang, Ju Huang, Jing Li, Jianguo Hu, Zhijun Geng","doi":"10.12122/j.issn.1673-4254.2026.06.05","DOIUrl":"10.12122/j.issn.1673-4254.2026.06.05","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the protective effect of 1,3-dicaffeoylquinic acid (1,3-DA) against dextran sulfate sodium (DSS)-induced colitis in mice and its molecular mechanism.</p><p><strong>Methods: </strong>Fifty C57BL/6 mice were randomly divided into normal control group, DSS model group, 1,3-DA treatment group, PI3K inhibitor (LY294002), and 5-aminosalicylic acid (5-ASA; positive control) group. Except for those in the control group, the mice were given DSS to induce colitis and treated with daily intraperitoneal injections the indicated agents during modeling for 7 consecutive days. Colonic pathological phenotypes, inflammation, oxidative stress, and expressions of tight junction proteins and PI3K/Akt pathway proteins in the colon tissues of the mice were detected. In cultured intestinal epithelial NCM460 cells with H₂O₂-induced oxidative stress, the effects of 1,3-DA and 1,3-DA plus 740Y-P (a PI3K activator) were examined on intracellular oxidative stress and expressions of tight junction proteins.</p><p><strong>Results: </strong>Treatment of the mice with 1,3-DA significantly alleviated DSS-induced body weight loss, colon shortening, elevation of disease activity index and mucosal injury, downregulated interferon‑γ and myeloperoxidase, upregulated superoxide dismutase, catalase and glutathione peroxidase, reduced malondialdehyde, increased zonula occludens-1 and claudin-1, and inhibited overexpressions of phosphorylated PI3K (p-PI3K) and phosphorylated Akt (p-Akt). In NCM460 cells, treatment with 1,3-DA significantly reduced H₂O₂-induced reactive oxygen species accumulation, increased zonula occludens-1 and claudin-1 expressions, and lowered p-PI3K and p-Akt expression. The protective effects of 1,3-DA was obviously attenuated by treatment with 740Y-P.</p><p><strong>Conclusions: </strong>1,3-DA ameliorates DSS-induced colitis in mice and H₂O₂-mediated intestinal epithelial injury by inhibiting inflammation and oxidative stress and promoting repair of intestinal barrier function, which is closely related to inhibition of excessive PI3K/Akt pathway activation.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 6","pages":"1244-1255"},"PeriodicalIF":0.0,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13294746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318256","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":"[Impact of preoperative cardiology consultation on major adverse cardiac events in non-cardiac surgery patients: a retrospective cohort study].","authors":"Peiqi Wang, Kai Zhang, Haijun Wang, Lujia Yang, Yanhong Liu, Jiangbei Cao, Hao Li, Weidong Mi, Jingsheng Lou","doi":"10.12122/j.issn.1673-4254.2026.06.10","DOIUrl":"10.12122/j.issn.1673-4254.2026.06.10","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate whether preoperative cardiology consultation reduces the incidence of major adverse cardiac events (MACE) in patients undergoing non-cardiac surgeries.</p><p><strong>Methods: </strong>This cohort study was conducted among 7019 elderly patients (above 65 years) with abnormal ECGs undergoing non-cardiac surgeries. The main outcome was MACE occurrence within 30 days post-surgery. The patients were divided into model development and validation cohorts in a 7:3 ratio, and each cohort was categorized into two subgroups with high-risk and low-risk abnormal ECG. MACE prediction models were constructed for the subgroups, and their predictive power was evaluated using ROC curves; the value of preoperative cardiology consultation for reducing MACE was assessed using decision curve analysis.</p><p><strong>Results: </strong>Among the 4914 patients in the model development cohort, 61 of the 3010 patients with low-risk abnormal ECGs experienced MACE (2.0%), as compared with 59 out of 1904 patients (3.1%) in the high-risk group. The predictive model for MACE for the low-risk group contained 6 risk factors (AUC=0.772), and that for the high-risk group contained 5 risk factors (AUC=0.769). In patients with low-risk abnormal ECG, undergoing cardiovascular specialist consultation did not show significant benefits (the survival rate for predicting MACE was 0.02). However, in patients with high-risk abnormal ECG and those with low-risk abnormal ECG but having specific risk factors, undergoing cardiovascular specialist consultation showed significant benefits with survival rates for predicting MACE of 0.3 and 0.229, respectively.</p><p><strong>Conclusions: </strong>For patients with high-risk abnormal ECG and those with low-risk abnormal ECG and specific risk factors, preoperative cardiology consultation may help to reduce the occurrence of MACE following non-cardiac surgeries, but for patients with simple low-risk abnormal ECG cases without risk factors, preoperative cardiology consultation can be omitted, which does not affect the incidence of MACE but can improve medical efficiency.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 6","pages":"1301-1312"},"PeriodicalIF":0.0,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13294739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318264","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>Wenyang Huazhuo Tongluo</i> Formula promotes angiogenesis in systemic sclerosis dermal microvascular endothelial cells by regulating the Sema3A/Nrp1 pathway].","authors":"Kelei Guo, Yiyuan Wang, Yingli Li, Hong Zhang, Li Han, Ruijuan DU, Jingfeng Ouyang, Hua Bian","doi":"10.12122/j.issn.1673-4254.2026.06.12","DOIUrl":"10.12122/j.issn.1673-4254.2026.06.12","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effect of <i>Wenyang Huazhuo Tongluo</i> Formula (WHT) for promoting angiogenesis in systemic sclerosis (SSc) dermal microvascular endothelial cells and its possible mechanism.</p><p><strong>Methods: </strong>Wistar rats were gavaged with 15, 30, or 60 g/kg WHT and normal saline for 7 consecutive days to prepare low-, medium-, or high-concentration WHT-medicated sera and blank serum, respectively. Human dermal microvascular endothelial cells (HDMECs) in routine culture were treated with the sera from SSc patients to establish an SSc cell model. The cells were treated with the blank serum, low-, medium-, or high-concentration WHT-medicated sera, or blank serum combined with EGCG (a Sema3A inhibitor). The changes in cell proliferation, migration and angiogenesis were assessed using CCK-8 assay, wound-healing assay and Matrigel tube formation assay, and the mRNA and protein expressions of Sema3A, Nrp1, VEGFA, CD31 and α-SMA were analyzed using qRT-PCR and Western blotting.</p><p><strong>Results: </strong>HDMECs treated with the serum from SSc patients exhibited significantly reduced cell proliferation and migration rates, increased α-SMA, Sema3A and VEGFA protein and mRNA expression levels, decreased CD31 and Nrp1 protein and mRNA expression levels, and suppressed angiogenesis. In SSc serum-induced cells, treatments with low-, medium-, or high-concentration WHT-medicated sera or EGCG all significantly improved cell survival and migration rates, reduced α-SMA, Sema3A and VEGFA protein and mRNA expression levels, enhanced CD31 and Nrp1 protein and mRNA expressions, and promoted angiogenesis of the cells.</p><p><strong>Conclusions: </strong>WHT promotes angiogenesis of SSc sera-induced HDMECs by modulating the Sema3A/Nrp1 signaling pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 6","pages":"1323-1330"},"PeriodicalIF":0.0,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13294755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318217","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":"[Serum from rats with electroacupuncture activates the PI3K/Akt signaling pathway to improve synaptic plasticity in HT22 neurons with oxygen and glucose deprivation].","authors":"Xueke Shi, Tingyu Chen, Jing Gao, Mingli Wu, Ruiqing Li, Kaiqi Su, Zhuan Lü, Xiaolei Song, Xiaodong Feng","doi":"10.12122/j.issn.1673-4254.2026.06.20","DOIUrl":"10.12122/j.issn.1673-4254.2026.06.20","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the protective effects of sera from rats receiving electroacupuncture (EA) against oxygen and glucose deprivation/reoxygenation (OGD/R) injury in HT22 neurons and explore the involvement of the PI3K/Akt signaling pathway in this protective mechanism.</p><p><strong>Methods: </strong>Bioinformatics analysis was performed using public databases to identify stroke-related pathways. A rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) were treated with EA at \"Shenting\" and \"Baihui\" to prepare EA rat serum. HT22 neurons were subjected to OGD/R and treated with MCAO rat serum, EA rat serum, LY294002, or EA rat serum combined with LY294002. The changes in cell viability, apoptosis, and neuronal morphology were assessed using CCK-8 assay, TUNEL staining, and Nissl staining. Western blotting was used to detect PI3K/Akt phosphorylation and the expressions of the downstream proteins (p-mTOR/mTOR and Bcl-2) and synaptic proteins (NMDAR1 and PSD-95); the mRNA expressions of PI3K, Akt, NMDAR1, and PSD-95 were detected using RT-qPCR.</p><p><strong>Results: </strong>HT22 neurons with OGD/R injury treated with MCAO rat serum showed significantly decreased cell viability, increased apoptosis, and impaired neuronal morphology, which were obviously improved following treatment with EA rat serum but aggravated after LY294002 treatment. The protective effect of EA rat serum was significantly attenuated by application of LY294002. HT22 neurons treated with MCAO rat serum showed decreased p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR ratios with lowered expressions of Bcl-2, NMDAR1 and PSD-95, which were obviously upregulated by EA rat serum treatment but reduced after LY294002 treatment. The cells with the combined treatment showed intermediate expression levels of these molecules at both the mRNA and protein levels.</p><p><strong>Conclusions: </strong>Serum from rats receiving EA at \"Shenting\" and \"Baihui\" shows a protective effect against OGD/R injury in HT22 neurons, mediated possibly by activation of the PI3K/Akt signaling pathway and its downstream effectors and upregulation of synaptic plasticity-related molecules.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 6","pages":"1407-1415"},"PeriodicalIF":0.0,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13294729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318053","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":"[Chronic iron overload induces diminished ovarian reserve in mice <i>via</i> iron metabolism dysregulation-mediated oxidative stress and endocrine dysfunction].","authors":"Jing Yu, Jijun Chu, Chengcheng Liang","doi":"10.12122/j.issn.1673-4254.2026.06.11","DOIUrl":"10.12122/j.issn.1673-4254.2026.06.11","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the mechanism by which chronic iron overload induces diminished ovarian reserve (DOR) in mice.</p><p><strong>Methods: </strong>Forty female C57BL/6J mice with normal estrous cycles were randomly divided into 4 groups (<i>n</i>=10) for intraperitoneal injections of normal saline or iron dextran at 0.1, 0.5 or 1.0 g/kg once a week for 8 consecutive weeks. The changes in body weight and food intake of the mice were monitored weekly. Vaginal smears were used to assess estrous cycle changes of the mice, and wet weights of bilateral ovaries and uterus were recorded. Ovarian histopathology was evaluated by HE staining, iron deposition was detected by Prussian blue staining; serum levels of sex hormones (FSH, LH, E₂, and AMH) and the levels of MDA and SOD in the ovarian tissue were determined, and reactive oxygen species (ROS) production was assessed on frozen sections of the ovarian tissue. Mitochondrial ultrastructural changes in the ovaries of the mice were observed with transmission electron microscopy, and ovarian expression levels of <i>Fth1</i>, <i>Ftl</i>, <i>Cat</i>, <i>Gpx1</i>, <i>Tf</i> and <i>Tfr1</i> mRNAs and Tf, Tfr1, Ft, Fth1, Ftl and Gpx4 protein were detected.</p><p><strong>Results: </strong>The mice receiving injections of 0.5 and 1.0 g/kg iron dextran exhibited disrupted estrous cycles, increased atretic follicles, decreased ovarian index, and increased uterine index with reduced AMH and E₂ levels and increased FSH and LH levels. The injections caused significant iron accumulation, oxidative stress, and obvious mitochondrial damage in the ovarian tissues, resulting also in downregulation of Tf, Tfr1, Gpx4, Gpx1 and Cat and upregulation of Ft, Ftl and Fth1 expressions.</p><p><strong>Conclusions: </strong>Iron dextran at 0.5 and 1.0 g/kg can induce chronic, dose-dependent iron overload in mice, which causes systemic iron metabolism disorders and disrupted iron homeostasis to trigger oxidative stress damage and endocrine dysfunction and ultimately induce DOR.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 6","pages":"1313-1322"},"PeriodicalIF":0.0,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13294749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318254","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":"[Ultrasound-synergized targeted nanoparticles suppress proliferation, migration and invasion of hypoxic lung cancer cells <i>in vitro</i>].","authors":"Junyu Dong, Jiajun Guo, Dairong Li, Yonghong DU","doi":"10.12122/j.issn.1673-4254.2026.06.08","DOIUrl":"10.12122/j.issn.1673-4254.2026.06.08","url":null,"abstract":"<p><strong>Objectives: </strong>To construct AS1411 aptamer-modified mesoporous polydopamine (MPDA) nanoparticles co-loaded with doxorubicin (DOX) and catalase (AS1411-D/C-MPDA nanoparticles) targeting the tumor microenvironment and evaluate their efficacy in synergy with ultrasound for inhibiting Lewis lung carcinoma (LLC) cells.</p><p><strong>Methods: </strong>AS1411-D/C-MPDA nanoparticles were synthesized using a one-step assembly method, and their physicochemical properties were characterized. Cultured LLC cells were treated with free DOX, DOX-loaded MPDA nanoparticles or AS1411-D/C-MPDA nanoparticles with or without ultrasound exposures (frequency 1.0 MHz and intensity 1.0 W/cm²) for 3 min. The changes in viability, apoptosis, and migration and invasion abilities of the cells were assessed using CCK-8 assay, flow cytometry (Annexin V-FITC/PI staining), wound healing assay, and Transwell assay, respectively.</p><p><strong>Results: </strong>The prepared AS1411-D/C-MPDA nanomaterials showed a uniform spherical morphology, a mean particle size of 183.36±15.99 nm, and DOX and catalase encapsulation efficiencies of (91.17±0.08)% and (29.59±0.2)%, respectively. The nanoparticles demonstrated good pH responsiveness to enable disintegration for promoting drug release, with a cumulative DOX release rate of (81.25±1.61)%. The nanoparticles possessed strong oxygen-generating capacity to alleviate cell hypoxia. AS1411-modified nanoparticles showed significantly enhanced cellular uptake by LLC cells. Compared with free DOX and DOX-MPDA nanoparticles combined with ultrasound, AS1411-D/C-MPDA in synergy with ultrasound induced higher levels of ROS in LLC cells, resulted in a higher cell apoptosis rate, and more efficiently reduced cell viability and suppressed cell migration and invasion.</p><p><strong>Conclusions: </strong>AS1411-D/C-MPDA nanoparticles combined with ultrasound allow targeted delivery of anticancer drugs and represent a promising strategy for synergistic treatment of lung cancer by integrating physical acoustics, pharmaceutical chemistry, and tumor microenvironment regulation.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 6","pages":"1278-1289"},"PeriodicalIF":0.0,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13294738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318121","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":"[Establishment of an gastric dysfunction and depression comorbidity model simulating clinical etiology in mice using a combined stress protocol].","authors":"Qingyang Huang, Wenwen Shen, Jin Hu, Hongkun Ma, Yanbing Hu, Chengjie Zhang, Guoming Shen, Hao Wang","doi":"10.12122/j.issn.1673-4254.2026.05.09","DOIUrl":"10.12122/j.issn.1673-4254.2026.05.09","url":null,"abstract":"<p><strong>Objectives: </strong>To establish a mouse model with the comorbidity of gastric dysfunction and depression mimicking clinical onset of the condition.</p><p><strong>Methods: </strong>Thirty male C57BL/6J mice were randomly divided into control, 14-day model, and 28-day model groups (<i>n</i>=10). The mice in the latter two groups were subjected to continuous combined stresses induced by tail clamping, cold-saline gavage and irregular feeding for 14 or 28 days. Gastric motility, gastric emptying and histopathological changes of the mice were evaluated using strain gauge sensors, <i>in vivo</i> imaging and HE staining, respectively, and behavioral tests were used to assess their depression-like behaviors. Serum corticotropin-releasing factor (CRF), brain-derived neurotrophic factor (BDNF), gastrin, motilin, and gastric nitric oxide synthase (NOS) and acetylcholinesterase (AChE) levels were measured by ELISA to explore the peripheral mechanisms.</p><p><strong>Results: </strong>Compared with control mice, the mice in 14-day model group exhibited reduced body weight, food intake and gastric motility amplitude with delayed gastric emptying but showed no significant depression-like behaviors; in 28-day model group, these changes were further exacerbated, and significant depression-like behaviors were observed. Compared with 14-day model group, the 28-day model group displayed severer gastric dysfunction and depression-like behaviors. Compared with control group, exposure to complex stresses for 14 days significantly increased serum CRF and decreased BDNF, gastrin and motilin levels, increased gastric NOS and decreased gastric AChE level, which were worsened after a 28-day exposure. HE staining showed no obvious histological changes in the gastric mucosa in the two model groups.</p><p><strong>Conclusions: </strong>Combined stresses induced by tail clamping, cold-saline gavage and irregular feeding for 28 days can induced the comorbidity of gastric dysfunction and depression in mice, and abnormal changes in serum neurotransmitters, brain-gut peptides and vagus activity may partly participate in the pathogenesis of the comorbidity.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"46 5","pages":"1059-1065"},"PeriodicalIF":0.0,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13213362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148033010","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}