Nan Fang Yi Ke Da Xue Xue Bao = Journal Of Southern Medical University[JOURNAL]
Sun
200 papers
[Erianin inhibits proliferation and migration of breast cancer cells by inhibiting Wnt/β-catenin signaling].
Fan D, Li X, Yao T … +3 more , Jin C, Wang X, Huang C
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045034 · Full text
OBJECTIVES: To investigate the effect of erianin on proliferation, migration, invasion, and apoptosis of breast cancer cells and the underlying mechanisms. METHODS: Breast cancer cell lines T-47D and MCF-7 treated with 0...
OBJECTIVES: To investigate the effect of erianin on proliferation, migration, invasion, and apoptosis of breast cancer cells and the underlying mechanisms. METHODS: Breast cancer cell lines T-47D and MCF-7 treated with 0, 12.5, 25, 50, and 100 nmol/L erianin for 12, 24, 36, 48, and 72 h were examined for cell viability using CCK-8 assay. The effects of erianin on cell proliferation, migration, invasion, senescence and apoptosis were evaluated using clone formation, wound healing, Transwell invasion, and senescence assays and flow cytometry. mRNA microarray analysis and the Enrichr database were used to explore the biological functions of erianin. Western blotting was used to detect the changes in protein expressions related to apoptosis, epithelial-mesenchymal transition (EMT), and the Wnt/β-catenin pathway. RESULTS: Erianin concentration-dependently inhibited cell viability, proliferation, migration, and invasion, and promoted senescence in T-47D and MCF-7 cells. Microarray analysis identified 1064 differentially expressed genes (DEGs), including 948 upregulated and 116 downregulated genes, which were involved primarily in EMT regulation, collagen-containing extracellular matrix, calcium ion binding, the PI3K-Akt signaling pathway, the Wnt/β-catenin signaling pathway, and apoptosis. Flow cytometry confirmed that erianin concentration-dependently induced apoptosis in the breast cancer cells, upregulated the expressions of Bax and caspase-3, decreased Bcl-2 expression, and lowered the expressions of EMT-related proteins (Snail, N-cadherin, and β‑catenin) and Wnt/β‑catenin signaling proteins (TCF4, Cyclin D1, and c-Myc). In the breast cancer cells treated with 100 nmol/L erianin, the application of a Wnt/β‑catenin agonist significantly increased the proteins expressions of TCF4, Cyclin D1, and c-Myc. CONCLUSIONS: Erianin inhibits proliferation, migration, and invasion and induces senescence and apoptosis in breast cancer cells possibly by suppressing the Wnt/β-catenin signaling pathway to induce cell apoptosis and reverse EMT of the cells.
[Ursolic acid in Formula inhibits colorectal cancer cell growth by inducing cuproptosis].
Jin C, Hong Z, Duan X … +5 more , Fan H, Yang J, Qin J, Zou L, Qin M
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045033 · Full text
OBJECTIVES: To investigate the molecular mechanism by which Formula (HJF) and its active component ursolic acid inhibit colorectal cancer (CRC) cell growth. METHODS: Proteomics was used to analyze the effect of HJF on p...
OBJECTIVES: To investigate the molecular mechanism by which Formula (HJF) and its active component ursolic acid inhibit colorectal cancer (CRC) cell growth. METHODS: 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. RESULTS: 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. CONCLUSIONS: As one of the key active components in the HJF, ursolic acid inhibits CRC cell growth by inducing cuproptosis targeting FDX1.
[Glutamine-induced autophagy exacerbates muscle atrophy in cachectic nude mice: a multi-omics analysis].
Li Z, Su X, Tian Z … +3 more , Chao X, Wang Y, Ma D
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045032 · Full text
OBJECTIVES: To clarify whether glutamine induces autophagy to promote skeletal muscle atrophy in cancer cachexia through integrated transcriptomic and metabolomic analyses. METHODS: Twenty male BALB/c nude mice were rand...
OBJECTIVES: To clarify whether glutamine induces autophagy to promote skeletal muscle atrophy in cancer cachexia through integrated transcriptomic and metabolomic analyses. METHODS: Twenty male BALB/c nude mice were randomized into control and model groups (=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. RESULTS: 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. CONCLUSIONS: 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.
[Ophiopogonin D alleviates doxorubicin-induced myocardial hypertrophy in mice by activating the β-catenin/FUNDC1/mitophagy axis].
Lei Y, Song J, Xu L … +2 more , Liu R, Zhao Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045031 · Full text
OBJECTIVES: To investigate whether ophiopogonin D (OD) alleviates doxorubicin (Dox)‑induced myocardial hypertrophy in mice by regulating the β‑catenin/FUNDC1/mitophagy signaling axis. METHODS: Thirty C57BL/6J mice were r...
OBJECTIVES: To investigate whether ophiopogonin D (OD) alleviates doxorubicin (Dox)‑induced myocardial hypertrophy in mice by regulating the β‑catenin/FUNDC1/mitophagy signaling axis. METHODS: Thirty C57BL/6J mice were randomized equally into control group, Dox treatment group, Dox with OD treatment group, Dox treatment group with injection of adeno-associated virus (AAV) vector carrying β‑catenin, and Dox treatment group with injection of AAV vector. RNA sequencing analysis was used to identify differentially expressed genes in cultured mouse cardiac cells following Dox treatment. Western blotting was performed to examine the protein levels of β‑catenin, active β‑catenin, FUNDC1, LC3, p62, β‑myosin heavy chain (β-MHC), and α‑actin; immunohistochemistry and immunofluorescence staining were used to assess the localization and expression of β-catenin and FUNDC1. Transmission electron microscopy was employed to evaluate mitochondrial damage in the cardiac myocytes. Chromatin immunoprecipitation and dual-luciferase reporter gene assays were used to investigate the transcriptional regulation of FUNDC1 by β‑catenin. RESULTS: Dox treatment significantly inhibited β‑catenin signaling and FUNDC1-mediated mitophagy, leading to cardiomyocyte hypertrophy and mitochondrial damage. OD treatment obviously reversed these effects, restored β‑catenin signaling, enhanced FUNDC1 transcription and expression, and promoted mitophagy. Overexpression of β‑catenin or FUNDC1 mimicked the cardioprotective effect of OD, while knockdown of β‑catenin aggravated myocardial hypertrophy, which was reversed by FUNDC1 overexpression. Mechanistically, β‑catenin directly bound to the FUNDC1 promoter and activated its transcription. CONCLUSIONS: OD alleviates Dox-induced myocardial hypertrophy in mice by activating the β‑catenin/FUNDC1/mitophagy axis and enhancing mitochondrial quality control.
[Patient and family predictors of group intervention outcomes in children with attention-deficit/hyperactivity disorder: a multidimensional model analysis].
Yang X, Wang Y, Mo X … +16 more , Zhu Z, Hong D, Hu Y, Peng K, Xu Y, Liu J, Guo W, Lin Q, Mai J, Mai S, Lu J, Yang C, Zhou Y, Cheng D, Yu M, Yin W
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045030 · Full text
OBJECTIVES: To explore individual and family characteristics associated with children's response to group interventions for attention-deficit/hyperactivity disorder (ADHD) based on multidimensional indicators of interven...
OBJECTIVES: To explore individual and family characteristics associated with children's response to group interventions for attention-deficit/hyperactivity disorder (ADHD) based on multidimensional indicators of intervention outcomes. METHODS: A total of 62 children with ADHD aged 6-9 years participating in an intervention program at the Affiliated Brain Hospital of Guangzhou Medical University from July 2023 to January 2025 were enrolled. All the participants received a standardized group intervention consisting of 8 sessions delivered over 4-6 weeks, focusing on attention training and emotion regulation training. Pre- and post-intervention data were collected using the General Information Questionnaire, the Difficulties in Emotion Regulation Scale (DERS), the Affective Reactivity Index (ARI), the Matson Evaluation of Social Skills with Youngsters (MESSY), and the parent-rated Swanson, Nolan, and Pelham Rating Scale-IV (SNAP-IV). Given the consistency in intervention format and structure between the two groups, data were pooled for modeling analyses. Changes in emotion regulation, inattention, and social skills were used as the outcome indicators. LASSO regression was used to screen 18 baseline variables (8 psychosocial characteristics and 10 demographic and family-background variables), followed by multiple linear regression to identify stable predictors. RESULTS: Across the models predicting changes in inattention, irritability, emotion-regulation difficulties, and inappropriately assertive/overconfident, the baseline score of each outcome was a significant positive predictor (β=0.462-0.669, _BH<0.05). Higher baseline hostile scores predicted less improvement in emotion-regulation difficulties (β=-0.326, _BH<0.01) and inappropriate assertiveness/overconfidence (β=-0.543, _BH<0.05). CONCLUSIONS: This study provides preliminary evidence that baseline symptoms and hostility traits may predict response to group interventions for ADHD, which may help to estimate treatment outcomes before intervention and provide support to precision intervention for children with ADHD.
[ Formula improves renal damage in mice with systemic lupus erythematosus by inhibiting p53-MDM2 signaling axis-mediated ferroptosis].
Li Y, Huang C, Pang L … +2 more , Zhu Z, Li M
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045029 · Full text
OBJECTIVES: To investigate the therapeutic mechanism of Formula (JPZS) for ameliorating renal injury in mice with systemic lupus erythematosus (SLE). METHODS: Thirty MRL/lpr lupus mice were randomly divided into model g...
OBJECTIVES: To investigate the therapeutic mechanism of Formula (JPZS) for ameliorating renal injury in mice with systemic lupus erythematosus (SLE). METHODS: Thirty MRL/lpr lupus mice were randomly divided into model group, JPZS treatment group, and prednisone treatment group, with 10 C57BL/6 mice as the control group. After treatment with daily gavage with normal saline, JPZS (7.8 g/kg) or prednisone (5 mg/kg) for 8 consecutive weeks, the mice were examined for changes in serum levels of anti-ds DNA, C3 and Scr, 24-h urine protein (24hPRO) and renal Fe content, MDA level, SOD activity, GSH level, and ROS level. Renal histopathological changes and ultrastructural changes were observed with HE staining and transmission electron microscopy. The changes in renal expressions of p53, MDM2, GPX4, SLC7A11, ACSL4, Bax, Bcl-2, and caspase-3 mRNAs and proteins were detected using RT-qPCR and Western blotting. RESULTS: Compared with the normal control mice, the mouse models of SLE had significantly elevated levels of dsDNA, Scr, 24hPRO, Fe²⁺, MDA, and ROS, increased renal expressions of p53, MDM2, ACSL4, Bax, and caspase-3, lowered levels of C3, SOD, and GSH, and reduced renal expressions of GPX4, SLC7A11, and Bcl-2 at both the mRNA and protein levels. Treatment with JPZS and prednisone both significantly ameliorated these abnormalities in the mouse models. CONCLUSIONS: JPZS can reduce renal ferroptosis in lupus mice, ameliorate kidney injury, and promote renal function repair possibly by inhibiting the p53-MDM2 signaling axis, which is closely associated with regulation of glomerular podocyte ferroptosis.
[Key determinants of global burden of non-alcoholic fatty liver disease: machine learning combined with Mendelian randomization analysis based on GBD data].
Chen H, Li Z, Ji M … +5 more , Wang X, Chen B, Guan Q, Wu M, Lu L
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045028 · Full text
OBJECTIVES: To analyze the global trends, drivers, and health inequalities of non-alcoholic fatty liver disease (NAFLD) burden to identify key predictors of NAFLD-related mortality. METHODS: Using data from the Global Bu...
OBJECTIVES: To analyze the global trends, drivers, and health inequalities of non-alcoholic fatty liver disease (NAFLD) burden to identify key predictors of NAFLD-related mortality. METHODS: Using data from the Global Burden of Disease (GBD) Study 2021, we extracted global measures of NAFLD from 1990 to 2021, and the trends were analyzed using joinpoint regression. Decomposition analysis was used to quantify the contributions of population growth, aging, and epidemiological changes. The health inequality was assessed using the concentration index. Using XGBoost-SHAP machine learning, the mortality predictors were identified, and two-sample Mendelian randomization was employed to test the causality for the key factors. All the analyses were conducted with data stratification by sex and the socio-demographic index (SDI). RESULTS: The global age-standardized disability-adjusted life years (DALYs) rate showed an increasing trend in both males (average annual percentage change [AAPC]=+0.34%) and females (AAPC=+0.05%). Decomposition analysis revealed that population growth was the primary driver of the global increase in DALYs, while population aging contributed to 52.37% of male deaths in high-SDI regions. Health inequality analysis showed a concentration index of -0.05 for DALYs in 2021, indicating a concentration of burden among low-SDI populations. Machine learning identified smoking (relative importance=100%) and advanced age (70-74 years: 60%) as the most critical predictors of mortality, and the model demonstrated good fit on the test set (=0.98). SDI-stratified analysis showed smoking and aging are the top two predictors across all SDI regions. Mendelian randomization further confirmed positive causal associations of smoking initiation (OR=1.35, <0.05) and aging (proxied by frailty index, OR=2.01, <0.05) with NAFLD risk. CONCLUSIONS: NAFLD burden is heavy globally with significant sex and socioeconomic inequalities. Smoking and advanced age are key risk factors for NAFLD, calling for integrated interventions for tobacco control, geriatric health management, and health equity promotion.
[Dynamic changes and physiological regulation of common carotid artery blood flow during general anesthesia in elderly patients: a prospective study].
Liu X, Wu J, Ye C … +2 more , Wang E, Hu H
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045027 · Full text
OBJECTIVES: To explore the dynamic pattern and physiological regulation of common carotid artery (CCA) blood flow during general anesthesia in elderly patients. METHODS: A total of 193 elderly patients undergoing abdomin...
OBJECTIVES: To explore the dynamic pattern and physiological regulation of common carotid artery (CCA) blood flow during general anesthesia in elderly patients. METHODS: A total of 193 elderly patients undergoing abdominal surgery were prospectively enrolled. Respiratory and hemodynamic variables and anesthetic depth of the patients were recorded throughout the perioperative period. CCA blood flow was measured at predefined time points using vector flow imaging. Heart rate, mean arterial pressure, end-tidal carbon dioxide, and bispectral index were included in a linear mixed-effects model, with patient ID as a random effect, to explore the physiological determinants of intraoperative CCA blood flow. RESULTS: CCA blood flow showed clear stage-related changes during general anesthesia. The mixed-effects model explained 52.0% of the variation in CCA blood flow (adjusted ²=0.520, <0.001). Heart rate, mean arterial pressure, end-tidal carbon dioxide, and bispectral index were all significantly associated with CCA blood flow (all <0.001). The standardized model further showed that the strength of these associations differed, with flow-related factors showing a stronger effect than blood pressure or heart rate alone. Surgical approach and patient position had no significant effect on CCA blood flow. CONCLUSIONS: Intraoperative cerebral perfusion is not maintained by blood pressure alone but influenced jointly by ventilation, hemodynamic status, and anesthetic depth. Recognizing and managing these factors may help optimize cerebral perfusion during surgery.
[Aerobic exercise produces cardioprotective effects in mice by regulating the oxidative stress-inflammation-Hippo/YAP signaling axis].
Zhang G, Wei S, Wang H … +3 more , Xie Y, He H, Li R
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045026 · Full text
OBJECTIVES: To investigate the mechanism by which aerobic exercise improves transverse aortic constriction (TAC)-induced heart failure in mice. METHODS: Thirty male C57BL/6J mice were randomized into sham-operated group,...
OBJECTIVES: To investigate the mechanism by which aerobic exercise improves transverse aortic constriction (TAC)-induced heart failure in mice. METHODS: Thirty male C57BL/6J mice were randomized into sham-operated group, TAC model group, and TAC with aerobic exercise (TACE) group. The mice in TACE group underwent a 4-week progressive treadmill training starting on day 3 following TAC modeling. Echocardiography and Masson's trichrome staining were used to assess cardiac function and myocardial fibrosis of the mice, respectively, and serum levels of BNP, TNF-α, IL-6, IL-1β, MDA, SOD, and GSH-Px were measured using ELISA. The mRNA and protein expressions of Hippo-YAP pathway components in the myocardial tissue were detected using RT‑PCR and Western blotting, respectively. Bioinformatics analysis was performed to explore the correlations among the measured indicators. RESULTS: Compared with those in TAC group, the mice in TACE group showed significantly reduced heart weight and heart weight/body weight ratio, increased left ventricular ejection fraction, left ventricular fractional shortening, and E/A ratio, reduced myocardial fibrosis, decreased BNP expression in both the serum and myocardial tissue, lowered serum levels of TNF‑α, IL‑6, IL‑1β, and MDA, and increased SOD and GSH-Px activities. The mRNA expressions of Mst1, Lats1, Lats2, and YAP1 were significantly downregulated in TACE group as compared with those in TAC group. Western blotting revealed decreased total protein expressions of Mst1/2, Lats1/2, and YAP and increased expression levels of phosphorylated Lats1/2 and phosphorylated YAP in TACE group. Correlation analysis suggested significant associations of oxidative stress markers and inflammatory factors with the expressions of the Hippo-YAP pathway components. CONCLUSIONS: Aerobic exercise improves cardiac function and attenuates cardiac remodeling in mice with TAC-induced heart failure possibly by suppressing oxidative stress and inflammation and modulating the Hippo-YAP pathway.
[Long non-coding RNA LASTR promotes progression of head and neck squamous cell carcinoma by binding to miR-4476 and upregulating BCAM expression].
Wu B, Song R, Gao N … +4 more , Xing K, Zhang P, Qu M, Zhang H
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045025 · Full text
OBJECTIVES: To investigate the regulatory role and mechanism of long non-coding RNA LASTR in progression of head and neck squamous cell carcinoma (HNSCC). METHODS: LASTR expression in HNSCC and its correlation with patie...
OBJECTIVES: To investigate the regulatory role and mechanism of long non-coding RNA LASTR in progression of head and neck squamous cell carcinoma (HNSCC). METHODS: LASTR expression in HNSCC and its correlation with patient prognosis were analyzed using TCGA and GEO transcriptomic data, and its expression in HNSCC cell lines was validated by qPCR. In a loss-of-function HNSCC cell model with siRNA-mediated LASTR knockdown, the changes in cell proliferation, migration, and invasion were assessed by high-content counting, CCK-8 assay, ATP detection, and Transwell assay. Bioinformatic analysis was conducted to identify the target genes of LASTR, and their interactions with BCAM were verified by qPCR and immunoblotting. The LASTR-miR-4476-BCAM regulatory axis was confirmed with RNA pulldown and dual-luciferase assays. The functional role of BCAM was investigated, and rescue experiments were performed to determine if BCAM mediates the effects of LASTR expression modulation. RESULTS: LASTR was significantly upregulated in HNSCC tissues and cell lines, and its high expression was significantly correlated with poor patient prognosis. In HNSCC cells, LASTR knockdown significantly suppressed cell proliferation, migration, and invasion. Bioinformatic analysis revealed 78 candidate target genes of LASTR, enriched in pathways involving angiogenesis, hypoxia response, MAPK, ErbB, and Ras signaling. LASTR knockdown obviously decreased BCAM expression HNSCC cells. Mechanistically, LASTR upregulated BCAM by sequestering miR-4476. BCAM knockdown similarly suppressed malignant phenotypes of HNSCC cells, and its overexpression rescued the inhibitory effects of LASTR knockdown. CONCLUSIONS: LASTR is upregulated in HNSCC and associated with poor prognosis. High expression of LASTR promotes HNSCC progression by acting as a ceRNA for miR-4476 to upregulate BCAM, suggesting the role of LASTR and BCAM as potential biomarkers and therapeutic targets for HNSCC.
[ Lotus Seed Drink improves diabetic kidney disease in mice by regulating the KDM3C/SP1 signaling pathway].
Xie J, Luo Y, Xia J … +1 more , Wang M
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045024 · Full text
OBJECTIVES: To investigate the therapeutic effect of Lotus Seed Drink (QISD) on renal injury in mice with diabetic kidney disease (DKD) and its mechanism. METHODS: The immunogenes differentially expressed in renal tubul...
OBJECTIVES: To investigate the therapeutic effect of Lotus Seed Drink (QISD) on renal injury in mice with diabetic kidney disease (DKD) and its mechanism. METHODS: The immunogenes differentially expressed in renal tubular epithelial cells (HK-2) induced by late glycosylation end products were screened using GSE193192 dataset from GEO database and the pharmacological mechanisms were predicted. Male ICR mouse models of DKD established by high-fat feeding for 4 weeks and intraperitoneal streptozotocin injection for 5 days were randomized for treatment with low (14.46 g/kg), medium (28.92 g/kg) and high (57.84 g/kg) doses of QISD via gavage for 12 weeks, with dapagliflozin as the positive control drug (=8). Penal pathologies of the mice were observed by HE, PAS and Masson staining, and renal expression levels of KDM3C, SP1, TNF-α, and MCP-1 mRNAs and proteins were detected using RT-qPCR and Western blotting. In a HK-2 cell model of lipopolysaccharide (LPS)-induced inflammatory injury, the effects of small-molecule inhibitors were tested to explore the therapeutic mechanism of QISD against cell inflammation. RESULTS: QISD treatment significantly lowered serum levels of glycated serum protein, creatinine and urea nitrogen, reduced glycogen accumulation, attenuated glomerular hypertrophy, and decreased renal inflammatory infiltration in DKD mouse models. QISD also reduces the expression levels of KDM3C, SP1, TNF‑α and MCP-1 in the kidney tissues of the mice. In LPS-induced HK-2 cells, the application of JIB-04, an inhibitor of KDM3C, obviously suppressed the expression levels of the inflammatory factors including TNF‑α, MCP-1 and ICAM-1. CONCLUSIONS: QISD can ameliorate renal injury in DKD mice by inhibiting inflammatory response suppressing excessive activation of the KDM3C/SP1 signaling pathway.
miR-24-3p promotes spinal cord injury repair in rats by inhibiting ferroptosis targeting GSK-3β.
Wei D, Wang B, Gao J … +8 more , Zhai T, Bai X, Zhu J, Zhang C, Shi C, Hao Q, Chen C, Zhao L
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Apr · PMID 42045023 · Full text
OBJECTIVES: To investigate the molecular mechanism by which miR-24-3p promotes spinal cord injury (SCI) repair in rats. METHODS: The changes in spinal cord miR-24-3p expression was detected in a SD rat model of SCI with...
OBJECTIVES: To investigate the molecular mechanism by which miR-24-3p promotes spinal cord injury (SCI) repair in rats. METHODS: The changes in spinal cord miR-24-3p expression was detected in a SD rat model of SCI with qRT-PCR. Using a stereotaxic apparatus, miR-24-3p agomir or a negative control reagent was microinjected at 3 mm rostral and caudal to the SCI epicenter of the rats Motor function recovery of the SCI rats was evaluated with BBB scores, histopathological changes and Fe²⁺ content in the SCI area were examined with HE staining and a commercial assay kit, and the changes in iron deposition in the SCI area was observed using Prussian blue staining with DAB. Western blotting and immunofluorescence staining were used to detect expressions of glycogen synthase kinase-3β (GSK-3β) and ferroptosis-related proteins xCT and GPX4 in the injured tissue. The targeted regulatory relationship between miR-24-3p and GSK-3β was verified using dual-luciferase reporter assay. In PC12 cells with erastin-induced ferroptosis, malondialdehyde (MDA) content was detected and the expression levels of GSK-3β, xCT and GPX4 proteins were determined by Western blotting and immunofluorescence staining. RESULTS: The expression of miR-24-3p and protein levels of xCT and GPX4 were significantly decreased in the SCI area of the rat models. Treatment with miR-24-3p agomir significantly improved hindlimb motor function of the SCI rats, alleviated spinal cord pathologies, reduced Fe²⁺ content, iron deposition and GSK-3β protein expression, and upregulated xCT and GPX4 protein expressions in the SCI area. Dual-luciferase reporter assay confirmed targeted inhibition of GSK-3β by miR-24-3p. In erastin-induced PC12 cells, transfection with miR-24-3p mimics significantly decreased intracellular MDA content and GSK-3β protein expression and increased xCT and GPX4 protein levels, and these effects were enhanced by co-transfection with GSK-3β inhibitor. CONCLUSIONS: miR-24-3p promotes repair of SCI in rats by inhibiting ferroptosis via targeted suppression of GSK-3β.
[Folic acid supplementation alleviates high-salt diet-induced renal fibrosis in mice].
Tang F, Wang Y, Liang T … +3 more , He W, Lao H, Song J
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887710 · Full text
OBJECTIVES: To investigate the protective effect of 2-week dietary folic acid (FA) supplementation against renal fibrosis induced by high-salt (HS) diet in mice. METHODS: Twenty-eight mice were randomly divided into cont...
OBJECTIVES: To investigate the protective effect of 2-week dietary folic acid (FA) supplementation against renal fibrosis induced by high-salt (HS) diet in mice. METHODS: Twenty-eight mice were randomly divided into control, HS (8% NaCl) diet group, HS+low-dose FA (FA: 0.56 mg/kg) group and HS+high-dose FA (5.6 mg/kg) group. The changes in body weight, food intake, water consumption, tail artery systolic pressure, and heart rate of the mice were monitored, and serum levels of creatinine (SCr) and inflammatory cytokines (IL-1β, IL-6, and TNF-α) were measured. Renal histopathology of the mice was assessed using HE, periodic acid-Schiff (PAS), Masson, and Sirius red staining. Renal expressions of , , -, and - mRNAs and E-cadherin, vimentin, and α‑SMA proteins were detected using RT-qPCR and immunohistochemistry. RESULTS: In mice feeding a HS diet, FA supplementation significantly reduced their water intake, lowered tail artery systolic pressure, heart rate, renal index and serum SCr levels, reducing also serum levels of TNF‑α , IL-1β, and IL-6. Masson and Sirius red staining revealed markedly reduced glomerular and interstitial fibrosis indices in HS+low-dose FA group, while the mice in HS+high-dose FA group showed mixed fibrotic improvements. Immunohistochemical results demonstrated that FA significantly upregulated E-cadherin protein expression and suppressed vimentin expression in renal tissues. Both FA doses inhibited HS-induced mRNA and protein expressions of fibrosis markers (, and -), attenuated interstitial collagen deposition, and alleviated renal fibrosis. FA also upregulated renal E-cadherin mRNA expression, contributing to fibrosis mitigation. CONCLUSIONS: FA intervention ameliorates renal inflammation and delays fibrosis progression in HS-fed mice. Low-dose FA supplementation produces better protective effect than high-dose FA, likely mediated by regulation of renal -, , , and - expressions.
[Identification of efferocytosis-related genes in osteoarthritis and prediction of traditional Chinese medicines based on bioinformatics and machine learning].
Xiang K, Zhang X, Li Z … +3 more , Xu Z, Liu S, Chai Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887709 · Full text
OBJECTIVES: 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 poten...
OBJECTIVES: 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). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
[Revision and validation of Liebowitz Social Anxiety Scale for Children and Adolescents].
Sun Z, Li W, Tang X … +1 more , Yu M
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887708 · Full text
OBJECTIVES: To adapt the Liebowitz Social Anxiety Scale for Children and Adolescents (LSAS-CA) to Chinese cultural contexts and assess its reliability and validity among Chinese adolescents. METHODS: A total of 2103 voca...
OBJECTIVES: To adapt the Liebowitz Social Anxiety Scale for Children and Adolescents (LSAS-CA) to Chinese cultural contexts and assess its reliability and validity among Chinese adolescents. METHODS: A total of 2103 vocational high school students (917 males and 1186 females; mean age 16.73±1.24 years) in Guangdong Province completed an online survey using the LSAS-CA. Item analysis and psychometric evaluations were conducted. The concurrent validity of the scale was assessed using the Social Anxiety Scale for Adolescents (SAS-A), Patient Health Questionnaire (PHQ-9), and Post-Event Processing Inventory-Trait (PEPI-T), and its discriminant validity was examined using the Rosenberg Self-Esteem Scale (RSES). Three months later, 210 of the students were retested to examine the test-retest reliability of LSAS-CA. RESULTS: The Chinese LSAS-CA retained 24 items (12 social interaction and 12 performance situations) for assessing anxiety and avoidance with a total of 48 scored responses. Confirmatory factor analysis was used for comparing fitting of 4 competing models (unidimensional, two-factor, bifactor, and higher-order models), and the bifactor model showed the best fit: anxiety bifactor model (χ²=3168.263, df=224, χ²/df=14.144, RMR=0.022, GFI=0.875, AGFI=0.832, PGFI=0.653, NFI=0.931, TLI=0.921, CFI=0.936, and RMSEA=0.079); avoidance bifactor model (χ²=3144.601, df=216, χ²/df=14.558, RMR=0.019, GFI=0.875, AGFI=0.826, PGFI=0.630, NFI=0.944, TLI=0.933, CFI=0.948, and RMSEA=0.080). CONCLUSIONS: The revised Chinese version of LSAS-CA has acceptable reliability and validity in the context of Chinese culture and provides a more convenient measurement tool for Chinese researchers to study adolescent social anxiety.
[ Capsule inhibits JAK/STAT-driven synovial angiogenesis in rheumatoid arthritis by suppressing the LncRNA EBLN3P/miR-369-3p/NFIX axis].
Sun M, Wang Y, Liu F
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887707 · Full text
OBJECTIVES: To investigate the mechanism by which Capsule (HQC) inhibits synovial angiogenesis mediated by the JAK/STAT pathway in rheumatoid arthritis (RA). METHODS: An optimized co-culture model of RA-derived fibrobla...
OBJECTIVES: To investigate the mechanism by which Capsule (HQC) inhibits synovial angiogenesis mediated by the JAK/STAT pathway in rheumatoid arthritis (RA). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
[Silybin inhibits fibrosis after glaucoma filtration surgery in rabbits by promoting fibroblast autophagy].
Zhang Y, Shen Y, Tong X … +3 more , Duan Y, Luo Y, Guo W
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887706 · Full text
OBJECTIVES: To investigate the effect of silybin in inhibiting fibrosis after glaucoma filtration surgery and the underlying mechanism. METHODS: Twenty-five healthy rabbits undergoing unilateral trabeculectomy on the lef...
OBJECTIVES: To investigate the effect of silybin in inhibiting fibrosis after glaucoma filtration surgery and the underlying mechanism. METHODS: Twenty-five healthy rabbits undergoing unilateral trabeculectomy on the left eye were randomly assigned into 5 groups for treatment with subconjunctival injections of sterilized water (control) or 50, 100, 200, and 250 μmol/L silybin for 7 consecutive days. Postoperative intraocular pressure (IOP) and filtration bleb morphology (Krofeld classification) were monitored. On day 28, tissues samples were harvested from the operated eyes for HE staining, Masson's trichrome staining, and immunofluorescence detection of fibronectin and collagen I. In cultured rabbit Tenon's capsule fibroblasts with TGF‑β1-induced fibrosis, the effects of silybin on autophagy and apoptosis were analyzed using Western blotting (LC3II/LC3I ratio and p62 expression) and flow cytometry. RESULTS: From postoperative day 7 to day 21, the rabbits with silybin treatment showed significantly lower IOP than those in the control group, and in the 200 and 250 μmol/L silybin groups, IOP reduction was maintained up to postoperative day 28. From postoperative day 14 to day 21, silybin dose-dependently increased the formation rate of functional filtering blebs, the 200 and 250 μmol/L silybin groups maintained more than 40% functional filtering blebs from postoperative day 14 to day 28. HE staining revealed obviously lessened inflammatory cell infiltration in silybin treatment groups compared with that in the control group. Masson's trichrome staining showed progressively reduced fibroblast numbers and collagen deposition in the silybin groups. Immunofluorescence staining confirmed that silybin dose-dependently reduced fibronectin and collagen I-positive cells. In cultured rabbit Tenon's capsule fibroblasts, silybin treatment effectively reversed TGF-β1-induced fibroblast fibrotic phenotype, increased the LC3II/LC3I ratio, decreased p62 expression, and promoted apoptosis of the fibroblasts. CONCLUSIONS: Silybin significantly inhibits postoperative fibrosis in rabbit models of glaucoma likely by activating cellular autophagy and inducing apoptosis to reduce fibroblast activation.
[Niranthin ameliorates Crohn's disease-like colitis in mice via antagonizing intestinal epithelial cell apoptosis and regulating intestinal Th1/Th2 immune homeostasis].
Wen H, Lin J, Zuo L … +1 more , Liu M
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887705 · Full text
OBJECTIVES: To investigate the effect of niranthin (Nir) in mice with Crohn's disease (CD)‑like colitis and its therapeutic mechanism. METHODS: In a mouse model of CD-like colitis induced using 2,4,6-trinitrobenzene sulf...
OBJECTIVES: To investigate the effect of niranthin (Nir) in mice with Crohn's disease (CD)‑like colitis and its therapeutic mechanism. METHODS: In a mouse model of CD-like colitis induced using 2,4,6-trinitrobenzene sulfonic acid, the effects of niranthin on colitis symptoms were evaluated by measuring changes in disease activity index (DAI) score, body weight, colon length, and colonic pathologies. Intestinal barrier function and cell apoptosis were evaluated using AB-PAS staining, immunofluorescence staining, Western blotting, and TUNEL staining. The changes in Th1 and Th2 cells in the mesenteric lymph nodes and colonic TNF-α and IL-10 expression levels were determined with flow cytometry and ELISA. In lipopolysaccharide (LPS)-induced mouse colon organoids, the effects of niranthin on organoid budding number and barrier protein expressions were observed. Network pharmacology and experiments were employed to explore and verify the therapeutic mechanism of niranthin on colitis. RESULTS: In the mouse models of CD-like colitis, niranthin treatment obviously improved weight loss, DAI scores, and colorectal shortening and significantly reduced tissue inflammation scores, goblet cell loss, and intestinal epithelial cell apoptosis. Niranthin significantly increased the budding number in LPS-induced mouse colon organoids. In both mouse colon tissues and LPS-induced mouse colon organoids, niranthin obviously increased the expressions of ZO-1 and claudin-1, downregulated the expressions of cleaved caspase-3 and BAX, and upregulated Bcl‑2 expression. The niranthin-treated mouse models showed significantly ameliorated Th1/Th2 imbalance in the mesenteric lymph nodes, downregulated TNF‑α and upregulated IL‑10 levels in the colon tissues. Network pharmacology predicted that the therapeutic mechanism of niranthin for CD-like colitis involved the PI3K/AKT pathway, which was validated in the mouse models treated with niranthin and the PI3K/AKT pathway activator Recilisib. CONCLUSIONS: Niranthin ameliorates colitis in mice by antagonizing epithelial apoptosis and regulating Th1/Th2 balance via inhibiting the PI3K/AKT pathway.
[Volatile oil from Schott ameliorates tic disorder in rats by inhibiting TLR4/MyD88/NF-κB-mediated microglial polarization].
Feng P, Wang J, Chu J … +5 more , Wang H, Tian Y, Zhang J, Wang M, Wang Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887704 · Full text
OBJECTIVES: To investigate the mechanism by which Schott volatile oil (VOA) alleviates tic disorder (TD) in rats. METHODS: Forty-eight 3-week-old SD rats were randomly divided into blank group (=8) and TD model group wi...
OBJECTIVES: To investigate the mechanism by which Schott volatile oil (VOA) alleviates tic disorder (TD) in rats. METHODS: Forty-eight 3-week-old SD rats were randomly divided into blank group (=8) and TD model group with intraperitoneal injection of iminodipropionitrile (=40). The rat models were further randomized into 5 groups (=8) for treatment with daily gavage of saline (model group), tiapride (47.91 mg/kg) or VOA (51.12 mg/kg), intraperitoneal injection of TAK-242 (a TLR4 inhibitor; 3 mg/kg), or both VOA gavage and TAK242 injection for 28 days. Behavioral changes of the rats were assessed, and Nissl staining was used to observe neuronal morphology in the striatum. The levels of TNF-α, C1q, TGF-β, and VEGF in the serum and striatum were measured using ELISA. The mRNA and protein expressions of TLR4, MyD88, and NF‑κB p65 in the striatum were detected using RT-PCR and Western blotting, and NF‑κB p65 nuclear translocation and expressions of Iba1 (a MG-specific marker), CD86 and CD206 were analyzed using immunofluorescence staining. RESULTS: VOA treatment significantly reduced tic-like behavior scores and ameliorated striatal neuronal damage in the rat models, resulting also in lowered levels of TNF-α and C1q and increased levels of TGF-β and VEGF in both the serum and striatum, decreased mRNA and protein expression levels of TLR4, MyD88, and NF‑κB p65 in the striatum, and reduced nuclear translocation of NF‑κB p65. Immunofluorescence staining revealed significantly weakened expressions of Iba1 and CD86 and enhanced CD206 expression in the striatum of VOA-treated rats. All these ameliorative effects of VOA were significantly attenuated by treatment with TAK-242. CONCLUSIONS: VOA alleviates tic symptoms in rats by inhibiting microglia activation and polarization to reduce neuroinflammation possibly through suppression of the TLR4/MyD88/NF-κB signaling pathway.
[ mechanical testing and finite element analysis of a novel β-Titanium alloy pedicle screw-rod fixation system].
Li J, Liu Y, Wang D … +3 more , Li H, He X, Lu T
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887703 · Full text
OBJECTIVES: To compare the biomechanical properties of a novel Ti-3Zr-2Sn-3Mo-25Nb β‑titanium alloy and a traditional Ti-6Al-4V titanium alloy pedicle screw-rod fixation system in posterior lumbar interbody fusion (PLIF)...
OBJECTIVES: To compare the biomechanical properties of a novel Ti-3Zr-2Sn-3Mo-25Nb β‑titanium alloy and a traditional Ti-6Al-4V titanium alloy pedicle screw-rod fixation system in posterior lumbar interbody fusion (PLIF). METHODS: mechanical tests were conducted to evaluate the bending, tensile, compressive, and torsional performance of the β-titanium alloy screws, connecting rods, and the assembled screw-rod fixation system. Two PLIF finite element models were constructed to compare the effects of Ti-6Al-4V versus β-titanium screw-rod systems on range of motion (ROM) and stresses in the endplate and implants. RESULTS: tests showed that the β‑titanium alloy screw exhibited good resistance to bending (455.95±18.66 N) and torsion (9.03±0.20 N·m). The maximum tensile load of the β-titanium rod was 17 647.06±101.89 N, and the β-titanium screw‑rod system showed a maximum compressive load of 417.65±5.09 N and a maximum torque of 25.00±0.70 N·m. Compared with Ti-6Al-4V, the β‑titanium model showed a 2.6%-8.3% increase in ROM, and the peak stresses in the interbody bone graft, cage, and endplate increased by 1.4%-8.5%, 2.2%-9.4%, and 2.2%-10.1%, respectively, whereas the peak stresses at the bone-screw interface and within the screw-rod system decreased by 8.8%-23.7% and 19.0%-33.1%, respectively. CONCLUSIONS: The β‑titanium pedicle screw-rod fixation system exhibits good mechanical performance to provide stability comparable to the conventional Ti-6Al-4V system while markedly reducing stress concentration within the screw-rod construct, suggesting its great potential for clinical application.
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