Nan Fang Yi Ke Da Xue Xue Bao = Journal Of Southern Medical University[JOURNAL]
Sun
200 papers
[ Formula regulates immune microenvironment of liver cancer in mice by inhibiting overactivation of NF-κB signaling pathway].
Wang Z, Liu L, Shi M … +3 more , Hou Y, Dong L, Zhang G
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887702 · Full text
OBJECTIVES: To investigate the regulatory mechanism of Formula on immune microenvironment of hepatocellular carcinoma (HCC) in mice. METHODS: Forty male BALB/c mice bearing subcutaneous Hep3B cell xenografts were random...
OBJECTIVES: To investigate the regulatory mechanism of Formula on immune microenvironment of hepatocellular carcinoma (HCC) in mice. METHODS: Forty male BALB/c mice bearing subcutaneous Hep3B cell xenografts were randomized equally into model group (with normal saline treatment), Tablet group, and low- (0.5 g/kg), medium- (1 g/kg), and high-dose (2 g/kg) Formula groups. All the mice received daily gavage of the corresponding treatments for 28 consecutive days, and the changes in tumor weight and volume were recorded every 7 days, and tumor inhibition rate was calculated after the final administration. Histopathological changes in the tumor tissues were observed with HE staining, and polarization of M1/M2 macrophages was analyzed with flow cytometry. The mRNA and protein expressions of iNOS, Arg-1, p65, and p50 in the tumor tissues were detected using q-PCR and Western blotting, and CD86 and CD206 protein expressions were observed with immunofluorescence staining. Serum levels of IL-4, IL-6, IL-10, IFN‑γ, TNF‑α, and TGF‑β1 of the mice were measured using ELISA. RESULTS: The mice in the 3 Formula groups showed significant reductions in tumor weight and volume with decreased tumor cell count, increased tumor cell apoptosis, increased percentage of M1 macrophages, and decreased percentage of M2 macrophages. The treatment obviously upregulated CD86 and downregulated CD206 expression in the tumor tissue, lowered the protein and mRNA expressions of iNOS, Arg-1, p65, and p50, reduced serum levels of IL-4, IL-10, TNF‑α, and TGF-β1, and increased serum levels of IL-6 and IFN-γ in the tumor-bearing mice. CONCLUSIONS: Formula effectively inhibits Hep3B cell xenograft growth in mice and induces a shift of M1/M2 ratio by promoting M1 polarization, thereby ameliorating the immunosuppressive tumor microenvironment and enhancing anti-tumor immunity possibly in association with inhibition of NF-κB signaling pathway overactivation.
[Modified Powder alleviates cholesterol gallstones in mice with liver depression syndrome by regulating gut microbiota and bile acid metabolism].
Liang R, Wang H, Li Z … +3 more , Chen H, Wang Y, Min L
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887701 · Full text
OBJECTIVES: To investigate the therapeutic effect of modified (CHSGS) in mice with cholesterol gallstones (CS) and liver depression syndrome and its potential mechanism. METHODS: Sixty male C57BL/6 mice were randomly di...
OBJECTIVES: To investigate the therapeutic effect of modified (CHSGS) in mice with cholesterol gallstones (CS) and liver depression syndrome and its potential mechanism. METHODS: Sixty male C57BL/6 mice were randomly divided into blank group (=9) and model group (=51) with CS induced by high-lithogenic diet feeding. After verification of successful modeling in 3 mice, the remaining 48 mouse models were divided into CS group, CS-liver depression (CS-LD) group, CHSGS group, and ursodeoxycholic acid (UDCA) group, and the latter 3 groups were subjected to CS-LD modeling by chronic unpredictable mild stress (CUMS) and solitary raising and treated with saline, CHSGS or UDCA gavage for 3 weeks. The mice were assessed for general state, body weight, depressive behavior, ileal pathologies, biliary total cholesterol (TC) and total bile acid (TBA) levels, and ileal mRNA expressions of TGR5, GLP-1, and GLP-2 using q-PCR. 16S rDNA sequencing and metabolomics studies were used to analyze fecal microbiota and bile acids of the mice. RESULTS: Compared to the blank control and CS mice, the CS-LD mouse models showed decreased body weight, depressive behaviors, enlarged gallbladder with crystals, intestinal villi damage, increased biliary TC, decreased TBA, and increased ileal GLP-1/2 and TGR5 mRNA expressions, which were obviously improved by CHSGS treatment. Microbiota analysis revealed decreased alpha diversity in CS and CS-LD groups, with altered abundances of , , , and . Bile acid profiling revealed significant upregulation of TDCA, DCA, and GDCA in CS group and increased CA and 3-ketodeoxycholic acid levels in CS-LD group. Correlation analysis suggested positive correlations between pro-lithogenic bile acids and the harmful gut bacteria. CONCLUSIONS: Modified CHSGS alleviates liver depression and cholesterol gallstones in mice likely by ameliorating gut microbiota dysbiosis and bile acid metabolism disorders.
[Formononetin downregulates P53/SAT1/ACSL4 pathway-mediated ferroptosis to improve hypoxic-ischemic brain injury in neonatal mice].
Guo T, Chen B, Yang X … +6 more , Zhao Y, Li X, He J, Shi J, Zuo H, Li J
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887700 · Full text
OBJECTIVES: To investigate the neuroprotective effects of formononetin (FMN) against hypoxic-ischemic brain damage (HIBD) in neonatal mice and the underlying mechanism. METHODS: Twenty-four neonatal C57BL/6J mice were ra...
OBJECTIVES: To investigate the neuroprotective effects of formononetin (FMN) against hypoxic-ischemic brain damage (HIBD) in neonatal mice and the underlying mechanism. METHODS: Twenty-four neonatal C57BL/6J mice were randomly divided (=6) into sham-operated group, HIBD model group, HIBD+FMN-L (50 mg/kg) group, and HIBD+FMN-H (100 mg/kg) group. Mouse models of HIBD were established by left common carotid artery ligation followed by hypoxia (92% N₂, 8% O₂) for 40 min. FMN at the two doses was administered by intraperitoneal injection, and 3 days later, brain tissues from the cortical ischemic penumbra were collected for assessing expressions of ferroptosis-related proteins (P53, SAT1, and ACSL4) using Western blotting and immunofluorescence staining and for detecting the levels of Fe²⁺, superoxide, malondialdehyde (MDA), and glutathione (GSH). In cultured HT22 neurons with oxygen-glucose deprivation (OGD), the effects of 100 μmol/L FMN, 10 μmol/L Nutlin-3 (a P53 agonist), or their combination on expressions of ferroptosis proteins, intracellular Fe²⁺, reactive oxygen species (ROS), lipid peroxidation, GSH, mitochondrial membrane potential, and cell viability were evaluated. RESULTS: In the neonatal mouse models of HIBD, FMN treatment significantly suppressed the protein expression of P53, SAT1, and ACSL4, reduced Fe²⁺, ROS, and MDA levels and increased GSH content in the cortical ischemic penumbra. In HT22 neurons with OGD, FMN obviously alleviated OGD-induced ferroptosis as shown by lowered expressions of the key ferroptosis proteins, reduced Fe²⁺ accumulation and lipid peroxidation, and significant increases of GSH levels, mitochondrial membrane potential, and cell viability. Mechanistic experiments showed that activation of P53 signaling by Nutlin-3 markedly reversed the protective effects of FMN. CONCLUSIONS: FMN produces neuro-protective effects against HIBD in neonatal mice by mitigating neuronal ferroptosis, primarily through downregulation of the P53/SAT1/ACSL4 signaling pathway.
[Different Astragalus medicinal pairs improve diabetic nephropathy in mice by regulating lipid peroxidation through PTGS2].
Chen X, Jing Y, Liang H … +5 more , Zhong J, Chen Z, Peng Y, Dai J, Xiao Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887699 · Full text
OBJECTIVES: To explore the regulatory effects of 3 Astragalus herb pairs (Astragalus-Salvia miltiorrhiza, Astragalus-Rehmannia glutinosa, and Astragalus-Dioscorea opposita) in Granule on PTGS2-mediated lipid peroxidatio...
OBJECTIVES: To explore the regulatory effects of 3 Astragalus herb pairs (Astragalus-Salvia miltiorrhiza, Astragalus-Rehmannia glutinosa, and Astragalus-Dioscorea opposita) in Granule on PTGS2-mediated lipid peroxidation in mice with diabetic kidney disease (DKD). METHODS: Network pharmacology was used to screen active components and targets of Astragalus membranaceus, Salvia miltiorrhiza, Rehmannia glutinosa, and Dioscorea opposita in Granule to construct herb pair-active component-target networks, followed by intersection analysis with DKD-related targets for PPI network construction and enrichment analysis. Molecular docking was used to verify the binding of the key active components to PTGS2. In 25 C57BL/6J mouse models of streptozotocin-induced DKD, the therapeutic effects of treatments with saline, irbesartan, and the 3 Astragalus herb pairs (=5) for 8 weeks were tested, with 5 normal mice serving as the control group. RESULTS: Network pharmacology showed extensive intersections between the active components of each herb pair and DKD-related targets, with PTGS2 as the key target. The major active components exhibited good binding affinity to PTGS2. The DKD mouse models in Astragalus-Salvia miltiorrhiza and Astragalus-Rehmannia glutinosa groups, particularly those in the former group, showed significant improvements in body weight, fasting blood glucose, serum creatinine, urea nitrogen, and 24-h urinary albumin. The Astragalus-Dioscorea opposita pair only slightly improved blood glucose and creatinine without improving urea nitrogen or urinary albumin in the mouse models. The Astragalus-Salvia miltiorrhiza pair, but not the other two pairs, markedly reduced the elevation of PTGS2 expression, significantly enhanced SOD activity, reduced MDA content, and upregulated GPX4 expression in the mouse models, and the therapeutic effect was only moderate in Astragalus-Rehmannia glutinosa group and the poorest in Astragalus-Dioscorea opposita group. CONCLUSIONS: The 3 Astragalus herb pairs from Granule can improve DKD in mice by reducing PTGS2-mediated lipid peroxidation, and the Astragalus-Salvia miltiorrhiza pair shows the strongest efficacy.
[ Granules inhibits renal fibrosis in mice by regulating glycolytic reprogramming and H3K18 lactylation].
Chen Y, Wang W, Cheng M … +6 more , Zhang W, Gao Y, Hong X, Zhang L, Dai R, Wang Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887698 · Full text
OBJECTIVES: To investigate the effects of Granules (QSG) on folic acid (FA)-induced renal fibrosis in mice and TGF-β1-stimulated HK-2 cells and the underlying mechanism. METHODS: A mouse model of FA-induced renal fibros...
OBJECTIVES: To investigate the effects of Granules (QSG) on folic acid (FA)-induced renal fibrosis in mice and TGF-β1-stimulated HK-2 cells and the underlying mechanism. METHODS: A mouse model of FA-induced renal fibrosis were treated daily with QSG at 4.0 g·kg¹ gavage for 4 weeks. Renal histopathological changes were evaluated using HE and Masson staining, and renal expressions of fibrosis markers, key glycolytic pathway proteins, and histone lactylation-related proteins (Pan Kla, and lactylation sites of H3/H4) were detected using Western blotting. Renal expressions of α-SMA, FN, E-cad, LDHA, and H3K18 lactylation (H3K18la) were also examined with immunofluorescence staining. Serum creatinine (SCR) and blood urea nitrogen (BUN) were measured by ELISA, and renal lactate content was determined with colorimetric assay. In HK-2 cells stimulated with TGF-β1, the effects of QSG-medicated serum from SD rats on cell viability, proliferation, protein expressions of α‑SMA, E-cad, LDHA, and H3K18la, extracellular oxygen consumption rate (OCR), extracellular acidification rate (ECAR), and intracellular lactate levels were analyzed. RESULTS: The mouse models of renal fibrosis showed increased renal expressions of α‑SMA, FN, HIF-1α, HK2, PFKM, PKM2, LDHA, Pan Kla, and H3K18la, elevated serum SCR and BUN and renal lactate level, and decreased E-cad expression. QSG treatment effectively reversed these changes and alleviated renal fibrosis in the mouse models. Immunofluorescence staining showed that QSG treatment significantly reversed the elevation of renal α‑SMA, FN and LDHA expressions and reduction of LDHA/H3K18la co-localization, and enhanced E-cad expression. In HK-2 cells, TGF‑β1 treatment significantly reduced cell viability, proliferation and OCR, and increased ECAR, lactate, α‑SMA, LDHA, and H3K18la, which were all reversed by treatment with QSG-medicated serum. Exogenous lactate obviously reversed the inhibitory effects of QSG on these proteins. CONCLUSIONS: QSG alleviates renal fibrosis in mice by modulating glycolytic reprogramming, reducing lactate accumulation, and inhibiting H3K18la.
[Eurycomanone inhibits renal ischemia/reperfusion-induced mitochondrial dysfunction and inflammation in mice by binding to STAT3 to inhibit its phosphorylation].
Liu Z, Mao Z, You D … +6 more , Wang J, He Y, Yu Y, Wen Z, Fang H, He W
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887697 · Full text
OBJECTIVES: To investigate the mechanism of eurycomanone (EN) for ameliorating ischemia/reperfusion (IR)-induced acute kidney injury (AKI) in mice. METHODS: Twenty-four male C57BL/6J mice were randomly divided into 4 gro...
OBJECTIVES: To investigate the mechanism of eurycomanone (EN) for ameliorating ischemia/reperfusion (IR)-induced acute kidney injury (AKI) in mice. METHODS: Twenty-four male C57BL/6J mice were randomly divided into 4 groups (=6) for sham operation, IR modeling by bilateral renal pedicle clamping, or intraperitoneal injections of EN at 0.25 or 1.0 mg/kg for two days prior to surgery. Network pharmacology and molecular docking were used to identify the potential molecular targets and signaling pathways and evaluate the binding affinities. Renal function, histopathological changes, expression of tubular injury markers (KIM-1 and NGAL), phosphorylation levels of STAT3, PI3K, and JAK2, renal inflammation, mitochondrial biogenesis, and mitochondrial function of the mice were assessed. The interaction between EN and STAT3 was examined using surface plasmon resonance (SPR). Another 24 male C57BL/6J mice receiving sham operation, IR modeling, or EN or EN+ML115 (a STAT3 agonist) treatment prior to modeling (=6) were used to validate the role of STAT3 in EN-mediated renal protection. RESULTS: Both low- and high-dose EN significantly alleviated renal injury and improved renal function in mice with IR-induced AKI. The core targets of EN were associated with inflammation-related signaling pathways. EN treatment markedly reduced renal levels of IL-6, MCP-1, and TNF-αand decreased macrophage infiltration (F4/80-positive cells) in renal interstitial tissue of the mice. EN also significantly increased renal ATP content and mitochondrial DNA copy number (<0.05), and upregulated the expressions of PGC-1α, TFAM, and Nrf2 mRNAs and protein levels of PGC-1α and TOM20. Molecular docking identified STAT3 and PI3K as key molecular targets of EN. In mice with IR-induced AKI, EN significantly suppressed phosphorylation of STAT3 and PI3K in the renal tissues without affecting p-JAK2 levels. SPR analysis confirmed a direct and specific interaction between EN and STAT3. Notably, activation of STAT3 by ML115 significantly reversed the renoprotective effects of EN. CONCLUSIONS: EN mitigates IR-induced AKI in mice by directly binding to STAT3 to inhibit its phosphorylation, suppressing inflammation, and enhancing mitochondrial biogenesis and function, suggesting the potential of EN as a promising therapeutic candidate for IR-induced AKI.
[Analysis of potential association of alcohol exposure with femoral head osteonecrosis and construction of a diagnostic model using machine learning].
Tao H, Liang F, Huang W … +2 more , Fan S, Zeng P
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887696 · Full text
OBJECTIVES: To construct and validate a diagnostic model for osteonecrosis of the femoral head (ONFH) based on alcohol exposure-related genes using machine learning methods. METHODS: The transcriptomic data related to al...
OBJECTIVES: To construct and validate a diagnostic model for osteonecrosis of the femoral head (ONFH) based on alcohol exposure-related genes using machine learning methods. METHODS: The transcriptomic data related to alcohol exposure and ONFH were obtained from the GEO database for construction of a diagnostic model for ONFH. The differentially expressed genes (DEGs) of alcohol exposure and ONFH were identified, and functional enrichment analysis of the intersecting genes was performed. Single sample gene set enrichment analysis (ssGSEA) was used to quantify immune infiltration. A total of 113 combinations of 12 machine learning algorithms were tested on the training set, and 10-fold cross-validation was used to construct the diagnostic model of ONFH, which was validated on the test set. The expressions of the DEGs in the model were detected by qRT-PCR in alcohol-treated MC3T3-E1 cells to verify the reliability of the constructed model. The Enrichr platform was used to identify potential drugs for ONFH. RESULTS: Twenty-one intersecting DEGs closely related to alcohol exposure and ONFH were identified, which were also involved in immune processes. Immune infiltration analysis showed that the patients with alcohol exposure and ONFH had significant differences in immune cell infiltration compared with the healthy controls. The diagnostic model was constructed based on 8 genes (SOAT1, GMCL1, GMPR, CISD2, ST3GAL6, AHSP, UBL3, and PTPN12), which showed significant differential expressions in alcohol-treated MC3T3-E1 cells. Ten potential drugs for ONFH treatment were predicted. CONCLUSIONS: By integrating bioinformatics analysis and machine learning methods, a reliable model for diagnosing ONFH has been successfully constructed based on the DEGs shared by alcohol exposure and ONFH.
[A nomogram model for predicting MACE risk following primary percutaneous coronary intervention in STEMI patients: an exploratory study based on serum GSDMD].
Hu X, Wang W, Li H … +4 more , Chen Z, Zhou X, Yuan J, Chen L
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887695 · Full text
OBJECTIVES: To investigate the value of serum gasdermin D (GSDMD) level for predicting 30-day major adverse cardiovascular events (MACE) in patients following primary percutaneous coronary intervention (PPCI) for acute S...
OBJECTIVES: To investigate the value of serum gasdermin D (GSDMD) level for predicting 30-day major adverse cardiovascular events (MACE) in patients following primary percutaneous coronary intervention (PPCI) for acute ST-segment elevation myocardial infarction (STEMI) and construct a predictive nomogram. METHODS: A total of 100 STEMI patients undergoing PPCI were prospectively enrolled. Serum GSDMD levels of the patients were measured by ELISA before and on the second morning after PPCI and compared using Wilcoxon signed-rank test. The patients were divided into high-GSDMD and low-GSDMD groups based on the optimal cut-off value of postoperative GSDMD levels determined by the Youden index. During the 30-day follow-up, the patients were categorized into MACE group (=26) and non-MACE group (=74). The key predictors were selected using univariable and LASSO regression, followed by multivariable logistic regression to identify the independent risk factors. A nomogram was constructed and evaluated by ROC curve analysis, Bootstrap internal validation, Hosmer-Lemeshow test, calibration plots and decision curve analysis (DCA). RESULTS: Post-PPCI serum GSDMD levels were significantly elevated relative to the pre-PPCI levels (=-4.848, <0.001). The incidence of 30-day MACE was significantly higher in the high GSDMD group (=0.01). Post-PPCI GSDMD level was identified as an independent risk factor for short-term MACE. The final nomogram incorporated Killip classification, number of stents, albumin, and post-PPCI GSDMD and demonstrated good predictive performance with an AUC of 0.847 (<0.001, 95% : 0.759-0.936), a sensitivity of 84.6% and a specificity of 79.7%. All the validation analyses confirmed good predictive efficacy and clinical utility of the model. CONCLUSIONS: Elevated post-PPCI serum GSDMD level is an independent risk factor for 30-day MACE in STEMI patients. The nomogram model based on this biomarker provides a reliable tool for short-term risk stratification of these patients.
[-derived extracellular vesicles exacerbate progression of lupus nephritis by activating natural killer cells].
Xiao J, Jin L, Duan L … +2 more , Gong Y, Li H
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887694 · Full text
OBJECTIVES: To investigate the regulatory effects of -derived extracellular vesicles (-EVs) on natural killer (NK) cell activation and cytotoxic function and their role in progression of systemic lupus erythematosus (SLE...
OBJECTIVES: To investigate the regulatory effects of -derived extracellular vesicles (-EVs) on natural killer (NK) cell activation and cytotoxic function and their role in progression of systemic lupus erythematosus (SLE). METHODS: Peripheral blood and fecal samples were collected from 35 SLE patients and 38 healthy individuals to assess the number and proportion of peripheral T cells, B cells, and NK cells. Fecal DNA was extracted for PCR amplification of DNA fragments and quantitative analysis using agarose gel electrophoresis. -EVs isolated by ultracentrifugation and characterized using transmission electron microscopy, nanoparticle tracking analysis, and Western blotting were co-cultured with NK cells, whose activation status and cytotoxicity were evaluated in vitro using qPCR and flow cytometry. Twenty-four MRL/lpr mice were randomized into 3 groups (=8) for treatment with gavage of 100 μL PBS or 20 μg -EVs or SS-EVs in 100 μL PBS. Kidney pathology, immune complex deposition, and peripheral cytokine levels were assessed with HE staining, immunofluorescence staining, and ELISA. RESULTS: The number and proportion of peripheral NK cells were significantly reduced (<0.0001) and the fecal abundance of was markedly increased in positive correlation with SLEDAI scores (R²=0.8369) in SLE patients. studies showed that -EVs significantly upregulated NK cell-activating receptors and enhanced NK-mediated cytotoxicity. In MRL/lpr mice, -EV treatment markedly exacerbated renal inflammation, promoted C3 and IgG immune complex deposition, and significantly increased serum levels of IL-6, TNF-α, IL-8, and CCL20. CONCLUSIONS: is enriched in the gut of SLE patients and promotes NK-cell activation by releasing -EVs, which induce renal inflammation and immune complex deposition and contributes to SLE progression. and its EVs may represent novel therapeutic targets for treatment of SLE.
[Selenocystine inhibits colon cancer cell growth by promoting reactive oxygen species generation to trigger oxidative damage].
Song Q, Miao Y, Feng X … +6 more , Wang Y, Liu W, Wei Q, Yu X, Chen W, Fu X
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887693 · Full text
OBJECTIVES: To explore the molecular mechanism by which selenocystine (SeC) inhibits colon cancer cell growth . METHODS: Colon cancer cells (RKO, HCT-116, and LoVo) were cultured and treated with 5, 10, or 20 μmol/L SeC...
OBJECTIVES: To explore the molecular mechanism by which selenocystine (SeC) inhibits colon cancer cell growth . METHODS: Colon cancer cells (RKO, HCT-116, and LoVo) were cultured and treated with 5, 10, or 20 μmol/L SeC for 24 h and 48 h. MTT assay was used to detect the cell viability, and wound healing assay was used to examine changes in cell migration. Flow cytometry with PI staining was used to analyze cell cycle arrest and apoptosis. Fluorescence probes were employed to monitor reactive oxygen species (ROS) generation, mitochondrial morphology and membrane potential, and the changes in ferroptosis were evaluated by detecting malondialdehyde (MDA), glutathione (GSH) and ferrous ion (Fe) levels; Western blotting was used to detect the changes in protein expressions. RESULTS: SeC at all the 3 doses significantly inhibited proliferation and migration of colon cancer cells, down-regulated the expression of cell cycle-related proteins CDK2 and CDK4 and activated the apoptotic proteins PARP and caspase-9. Western blotting showed that SeC decreased the expression of ferroptosis proteins FTH1 and xCT and increased the expression of DMT1. The levels of MDA and Fe were increased and GSH level was decreased in SeC-treated cells. Fluorescence staining results showed that SeC treatment induced mitochondrial structure damages and promoted cellular ROS production. SeC treatment also increased phosphorylation of oxidative damage proteins and lowered the expression levels of NRF2 and HO-1 proteins. ROS scavenger significantly reversed the up-regulation of DMT1, PARP and p-HA.X protein induced by SeC in colon cancer cells. CONCLUSIONS: SeC induces apoptosis and ferroptosis of colon cancer cells by promoting ROS generation and initiating oxidative damage, suggesting the potential of SeC as a potential chemotherapeutic agent for colon cancer.
[ improves osimertinib resistance of non-small cell lung cancer cells by regulating the lactate/Wnt/β-catenin/LDHA pathway].
Liang Z, Pan F, Deng L … +4 more , Mai Z, Ma Y, Shi C, Fu W
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887692 · Full text
OBJECTIVES: To explore the effect of (SMS) for improving osimertinib resistance in non-small cell lung cancer cells and the underlying mechanism. METHODS: Cultured A549 cells were treated with osimertinib alone or in co...
OBJECTIVES: To explore the effect of (SMS) for improving osimertinib resistance in non-small cell lung cancer cells and the underlying mechanism. METHODS: Cultured A549 cells were treated with osimertinib alone or in combination with SMS-medicated rat serum, and the changes in cell viability and glucose and lactate levels were determined. The effect of SMS combined with osimertinib for improving osimertinib resistance of A549 cells was assessed in a mouse model bearing subcutaneous A549 cell xenograft. Western blotting, RT-qPCR, and immunofluorescence staining were used to analyze the effects of SMS and lactate on the Wnt/β‑catenin/LDHA signaling pathway. RESULTS: SMS significantly increased osimertinib sensitivity of A549 cells in a concentration-dependent manner. Compared with osimertinib alone, the combined treatment with SMS and osimertinib significantly inhibited cell viability, colony formation ability, and tumor growth in nude mice. SMS concentration-dependently decreased glucose and lactate levels in A549 cells. The results of Western blotting showed that SM inhibited the protein expression of LDHA, total β‑catenin, and cytoplasmic and nuclear β‑catenin, while lactate obviously activated the expressions of total β‑catenin protein, nuclear β‑catenin, and LDHA in A549 cells. Immunofluorescence concentration-dependent staining showed that lactic acid activated nuclear accumulation of β‑catenin protein, while SMS significantly inhibited the expression of nuclear β‑catenin protein; RT-qPCR demonstrated that lactate significantly increased mRNA expressions of the Wnt/β‑catenin downstream target genes (c-myc, CD44, Axin2, Oct3/4, survivin, and CCND1), while SMS inhibited their expressions. CONCLUSIONS: SMS improves osimertinib resistance in non-small cell lung cancer cells by inhibiting lactate/Wnt/β-catenin/LDHA pathway-mediated glycolysis.
[ alleviates bile duct ligation-induced hepatic fibrosis in rats by regulating the Sirt1-autophagy signaling pathway].
Li C, Cui L, Cao J … +4 more , Fan Y, Zhou X, Zhang S, Zuo Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887691 · Full text
OBJECTIVES: To investigate the protective effect of (HXQJL) agaisnt bile duct ligation (BDL)-induced liver fibrosis in rats and the underlying mechanism. METHODS: SD rats were randomized into sham-operated group, BDL mo...
OBJECTIVES: To investigate the protective effect of (HXQJL) agaisnt bile duct ligation (BDL)-induced liver fibrosis in rats and the underlying mechanism. METHODS: SD rats were randomized into sham-operated group, BDL model group, low- and high-dose HXQJL treatment groups, Ex527 (a Sirt1 inhibitor) group (EX527), and HXQJL+Ex527 group. Liver histopathological changes and collagen deposition were observed using HE and Sirius Red staining, and serum levels of ALT, AST, ALP, and GGT of the rats were measured using biochemical assays. The expression levels of α‑SMA, FN, COL I, Atg5, Beclin1, p62, LC3B, and Sirt1 were determined by RT-PCR and Western blotting. Immunofluorescence staining was used to detect the expression of α-SMA, LC3B, and Sirt1. RESULTS: Compared with the sham-operated rats, the rats in BDL model group exhibited increased hepatocyte injury, inflammatory cell infiltration, and collagen deposition area with elevated serum levels of ALT, AST, ALP, and GGT, enhanced haptic expressions of α‑SMA, FN, COL I, Atg5, and Beclin1, an increased LC3B-II/I ratio, and lowered hepatic expressions of p62 and Sirt1. All these changes were significantly alleviated in the two HXQJL treatment groups but aggravated in EX527 treatment group. Compared with those in high-dose HXQJL group, the protective effects of HXQJL on liver tissue injury, liver function, liver fibrosis, and autophagy were obviously mitigated by treatment with Ex527. CONCLUSIONS: HXQJL has protective effect against BDL-induced liver fibrosis in rats by modulating the Sirt1-autophagy signaling pathway.
[Intraperitoneal administration of Allium macrostemon-derived carbon quantum dots alleviates cisplatin-induced acute kidney injury and restores mitochondrial function in mice].
Yang J, Yang L, Hong K … +5 more , Geng B, Zhao M, Wang Y, Xia T, Dong J
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887690 · Full text
OBJECTIVES: To investigate the protective effects of carbon quantum dots (CQDs) derived from Allium macrostemon () administered orally or via intraperitoneal injection in a mouse model of cisplatin-induced acute kidney i...
OBJECTIVES: To investigate the protective effects of carbon quantum dots (CQDs) derived from Allium macrostemon () administered orally or via intraperitoneal injection in a mouse model of cisplatin-induced acute kidney injury (AKI) and explore the underlying mechanisms. METHODS: Male C57BL/6 mice were randomly divided into control group, AKI model group, intraperitoneal injection group, and oral administration group (=6). In all but the control group, the mice received a single intraperitoneal injection of cisplatin (20 mg/kg) on day 3 to induce AKI; intraperitoneal injections of -derived CQDs (0.25 mL/day) were administered on a daily basis for 5 consecutive days, and oral CQD solution was given at the dose of 1 mL/day. On day 6, blood samples were collected to measure serum creatinine (CRE) and blood urea nitrogen (BUN). HE staining and transmission electron microscopy (TEM) were used to evaluate kidney tissue structure, mitochondrial morphology, and podocyte injury. Expression levels of renal injury markers (KIM-1 and NGAL) and inflammatory cytokines (IL-6, TNF‑α, and IL-1β) were determined with with RT-qPCR and Western blotting. RESULTS: Compared with those in the control group, AKI mice exhibited significant weight loss, renal enlargement, increased kidney-to-body weight ratio, and elevated serum CRE and BUN levels. In both CQDs treatment groups, kidney/body weight ratios and serum CRE and BUN levels were reduced and the expression levels of KIM-1, NGAL, and inflammatory cytokines were lowered significantly. Histological and ultrastructural analyses revealed more intact renal architecture, reduced inflammatory infiltration, restored mitochondrial morphology, and alleviated podocyte foot process fusion and basement membrane thickening in the two treatment groups, particularly in the intraperitoneal injection group. CONCLUSIONS: Intraperitoneal administration of -derived CQDs effectively attenuates cisplatin-induced AKI in mice, improves renal function, suppresses inflammatory responses, and repairs mitochondrial damage, thus offering better renal targeting and protective effects for AKI prevention and treatment.
[Mefloquine HCl promotes DNA repair and alleviates radiation-induced lung epithelial cell injury].
Zhang Y, Wen Q, Huang H … +2 more , Zhou M, Wang J
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887689 · Full text
OBJECTIVES: To investigate the protective effect of mefloquine HCl (MQ) against X-ray irradiation-induced DNA damage in lung epithelial cells. METHODS: Human lung epithelial cells (BEAS-2B) were divided into blank contro...
OBJECTIVES: To investigate the protective effect of mefloquine HCl (MQ) against X-ray irradiation-induced DNA damage in lung epithelial cells. METHODS: Human lung epithelial cells (BEAS-2B) were divided into blank control group, irradiation group, and irradiation+MQ treatment group. The effects of MQ on cell proliferation and radiosensitivity after X-ray irradiation were assessed using CCK-8 assay, EdU-488 assay, and colony formation assay. Apoptosis and cell cycle distribution of BEAS-2B cells with different treatments were detected by flow cytometry. The effect of MQ in promoting DNA double-strand break (DSB) repair was observed using immunofluorescence staining and comet assay, and the molecule ar mechanism was explored using Western blotting, qPCR, and luciferase reporter assays. RESULTS: MQ at 0-10 μmol/L did not significantly affect BEAS-2B cell viability. Compared to the irradiated cells, treatment with 0-10 μmol/L MQ enhanced the cell viability, and the effect was the most conspicuous at 10 μmol/L. MQ treatment obviously promoted proliferation and increased clonogenic survival rate of irradiated BEAS-2B cells while reducing their radiosensitivity, and significantly lowered cell apoptosis rate following the irradiation. Cell cycle analysis revealed that MQ alleviated G2/M phase arrest induced by irradiation, and comet assay and immunofluorescence staining showed reduced comet tail moment and γH2AX foci formation in irradiation+MQ group. Western blotting and qPCR demonstrated that MQ treatment for 48 h significantly increased CtIP promoter activity and upregulated CtIP expressions at both the mRNA and protein levels. CONCLUSIONS: MQ promotes DSB repair in BEAS-2B cells by upregulating CtIP expression and may thus alleviate radiation-induced lung epithelial cell injury.
[Esketamine alleviates depression-like behaviors in mice with chronic restraint stress by activating glutamatergic neurons in the medial prefrontal cortex].
Zhang Z, Hao X, Cao F … +5 more , Guo Y, Guo S, Cai C, Mi W, Tong L
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887688 · Full text
OBJECTIVES: To investigate the regulatory role of glutamatergic neurons in the medial prefrontal cortex (mPFC) in the antidepressant effects of esketamine. METHODS: A total of 150 male C57BL/6J mice were randomly divided...
OBJECTIVES: To investigate the regulatory role of glutamatergic neurons in the medial prefrontal cortex (mPFC) in the antidepressant effects of esketamine. METHODS: A total of 150 male C57BL/6J mice were randomly divided into 15 groups (10). The mice subjected to the chronic restraint stress (CRS), and those exhibiting depressive-like behaviors following CRS received either esketamine or saline treatment, and subsequent behavioral changes were evaluated. Depressive-like behaviors were assessed using tail suspension test (TST), forced swim test (FST), and sucrose preference test (SPT). The changes in neuronal activity within the mPFC were examined using c-Fos immunofluorescence staining. To explore the underlying mechanism, chemogenetic approaches were employed to specifically modulate the activity of mPFC glutamatergic neurons and examine how these manipulations influenced the effect of esketamine on behaviors of the mice. RESULTS: Compared with saline-treated CRS mice, the mice with esketamine treatment showed significantly reduced immobility time in TST and FST and increased sucrose preference rate. Immunofluorescence staining revealed significantly increased expression of c-Fos in glutamatergic neurons in esketamine-treated mice. Chemogenetic activation of mPFC glutamatergic neurons (hM3Dq group) significantly decreased immobility time of the mice in the TST and FST and increased their sucrose preference as compared with the mice in mCherry group (<0.01), while inhibition of the mPFC glutamatergic neurons (hM4Di group) produced no significant effect. Among the mice treated with esketamine, those in hM4Di group exhibited significantly increased immobility time in TST and FST and decreased sucrose preference compared with those in mCherry group, while the mice in hM3Dq group showed no such changes. CONCLUSIONS: Esketamine produces antidepressant effects in mice with CRS by activating glutamatergic neurons in the mPFC.
[Tumor-secreted dentin sialophosphoprotein induces oxaliplatin resistance in colorectal cancer through an integrin αvβ3-dependent pathway].
Liu C, Ning Z, Wu J … +5 more , Liu W, Lin C, Xu J, Zhou R, Zhao L
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Mar · PMID 41887687 · Full text
OBJECTIVES: To determine whether dentin sialophosphoprotein (DSPP) modulates oxaliplatin efficacy for colorectal cancer (CRC) and explore the underlying integrin αvβ3-dependent mechanism. METHODS: Immunohistochemistry wa...
OBJECTIVES: To determine whether dentin sialophosphoprotein (DSPP) modulates oxaliplatin efficacy for colorectal cancer (CRC) and explore the underlying integrin αvβ3-dependent mechanism. METHODS: Immunohistochemistry was used to compare the expression levels of DSPP between oxaliplatin-sensitive and oxaliplatin-resistant CRC tissues. The changes in oxaliplatin sensitivity in parental and oxaliplatin-resistant CRC cell lines after DSPP knockdown or overexpression were assessed using CCK-8 assay, and Western blotting was used to evaluate the efficacy of DSPP modulation and MAPK pathway activity. The interaction between DSPP and integrin αvβ3 was examined by immunofluorescence staining, co-immuno-precipitation, and immunohistochemistry. HE and immunofluorescence staining were used to confirm the establishment of CRC organoid models. Patient-derived xenograft (PDX) and nude mouse subcutaneous xenografts were used to evaluate the in vivo effect of targeting DSPP on oxaliplatin response. RESULTS: DSPP expression was significantly elevated in oxaliplatin-resistant patients and in oxaliplatin-resistant HCT8 cells. DSPP knockout significantly increased oxaliplatin sensitivity in oxaliplatin-resistant HCT8 cells and in HCT116 and SW620 cells. Co-immunoprecipitation revealed binding between DSPP and integrin αvβ3 in tumor cells, and immunofluorescence staining demonstrated their co-localization. Immunohistochemistry showed a positive correlation between DSPP expression and integrin αvβ3 expression in CRC tissues. Western blotting indicated that DSPP upregulated the phosphorylation levels of ERK and P53 in the MAPK signaling pathway, whereas the integrin αvβ3-targeted inhibitor (Cyclo) effectively abrogated this regulatory effect. In the xenograft and PDX models, targeted inhibition of DSPP or integrin αvβ3 suppressed tumor growth and improved the efficacy of oxaliplatin, for which the anti-DSPP monoclonal antibody was more effective than integrin αvβ3-targeted inhibitor. CONCLUSIONS: We identified a DSPP-integrin αvβ3 axis that mediates oxaliplatin resistance, and DSPP may serve as a therapeutic target to restore chemosensitivity in advanced CRC.
[Research progress on the correlation between Akkermansia muciniphila and cardiovascular diseases].
Jiang S, Gong L, Zheng H
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633704 · Full text
Cardiovascular disease (CVD) is one of the leading causes of death globally, characterized by high morbidity and mortality rates. Metabolic disorders are critical risk factors for CVD. In recent years, growing evidence h...
Cardiovascular disease (CVD) is one of the leading causes of death globally, characterized by high morbidity and mortality rates. Metabolic disorders are critical risk factors for CVD. In recent years, growing evidence has highlighted the crucial role of gut microbiota in the onset, progression, and pathological mechanisms of both metabolic diseases and CVD. Akkermansia muciniphila (), a promising next-generation probiotic, has attracted considerable attention due to its unique metabolic functions and immunomodulatory properties. This review systematically summarizes the mechanisms and research progress regarding the role of in metabolic diseases and cardiovascular diseases. It elucidates how this bacterium exerts beneficial effects on metabolic disorders through multiple pathways, including improving gut barrier function, regulating lipid and glucose metabolism, increasing short-chain fatty acid production, and suppressing inflammatory responses. Meanwhile, is also involved in cardiovascular protective processes such as anti-atherosclerosis, blood pressure regulation, alleviation of atrial fibrillation, and improvement of pulmonary arterial hypertension. Its mechanisms involve immunomodulation, regulation of metabolites, and multi-level interactions along the gut-cardiovascular axis, offering novel microbial targets and strategies for intervening in related diseases.
[Comparison of missing data handling methods for AC coefficient estimation].
Li K, Xu L, Yu M … +1 more , An S
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633703 · Full text
OBJECTIVES: To explore the impact of different missing data handling methods on AC coefficient estimation through simulation studies. METHODS: Monte Carlo simulation was used to generate evaluation data under different m...
OBJECTIVES: To explore the impact of different missing data handling methods on AC coefficient estimation through simulation studies. METHODS: Monte Carlo simulation was used to generate evaluation data under different missing mechanisms. The parameters generated included the number of raters, categories, sample size, disease prevalence, random rating probability, and missing proportion. Four missing data handling methods, by excluding subjects with zero ratings, excluding subjects with incomplete ratings, rater mode imputation, and subject mode imputation, were compared using bias and mean squared error (MSE) as metrics. RESULTS: When disease prevalence was balanced or the missing data mechanism was missing completely at random (MCAR) or at random (MAR), excluding subjects with zero ratings showed the best performance, with bias and MSE close to zero at a missing proportion below 30%. Under skewed prevalence and missing not at random (MNAR), subject mode imputation was superior for AC coefficient estimation, resulting in a bias within ±0.10 and an MSE below 0.09; for a sufficient sample size and a missing proportion ≤30%, the MSE of this method was nearly zero. Rater mode imputation showed the worst performance across all these scenarios. Excluding subjects with incomplete ratings resulted in an acceptable error only in relatively simple settings (two raters and two categories) with low a missing proportion under MCAR/MAR, but showed a poor stability in other scenarios. CONCLUSIONS: No universally optimal method exists for handling missing data in AC estimation. We recommend excluding subjects with zero ratings for balanced prevalence or MCAR/MAR, and subject mode imputation for skewed prevalence under MNAR. Researchers should report AC estimates from multiple methods to allow assessment of result sensitivity.
[Drug repositioning prediction based on dynamic feature learning on heterogeneous graphs].
Zhu H, Guo Y, Xin X … +2 more , Li C, Zhou D
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633702 · Full text
OBJECTIVES: To address the challenges faced by existing artificial intelligence methods in modeling complex heterogeneous biological networks, particularly their limitations in capturing collaborative relationships betwe...
OBJECTIVES: To address the challenges faced by existing artificial intelligence methods in modeling complex heterogeneous biological networks, particularly their limitations in capturing collaborative relationships between nodes and in extracting high-order topological semantic features, we propose a novel drug repositioning prediction method based on dynamic representation learning on heterogeneous graphs. METHODS: A heterogeneous biological graph that integrates drugs, diseases, and their interaction relationships was constructed, based on which a dynamic gated attention module was designed to extract discriminative topological features of drugs and diseases by incorporating a dynamic graph attention mechanism. A gated residual feature fusion mechanism was developed to precisely integrate structural and semantic information from multiple similarity networks to reduce feature redundancy and information loss, thereby enabling accurate prediction of drug-disease associations. RESULTS: Experiments and case studies conducted on multiple drug datasets related to complex diseases demonstrated that the proposed method outperformed existing mainstream models in drug repositioning prediction. CONCLUSIONS: The proposed method can effectively model complex associations in heterogeneous biological networks, enhance the accuracy of drug repositioning prediction, and provide important technical support for precision treatment of complex diseases and development of medical artificial intelligence.
[Optimized extraction of active components of and their antioxidant, anti-inflammatory and pigmentation-reducing effects for skin whitening].
Xu Q, Li W, Zhang X … +4 more , Chen Y, Jiang Z, Li G, Yan M
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633701 · Full text
OBJECTIVES: To optimize the extraction process of the active components of Radix and assess the antioxidant, anti-inflammatory and pigmentation-reducing effects of Radix extract (BST). Methods docking identified galli...
OBJECTIVES: To optimize the extraction process of the active components of Radix and assess the antioxidant, anti-inflammatory and pigmentation-reducing effects of Radix extract (BST). Methods docking identified gallic acid, liquiritin, and paeoniflorin as potential tyrosinase inhibitors, and their contents in BST were determined with high-performance liquid chromatography (HPLC). Based on the contents of the 3 inhibitors, their tyrosinase-inhibiting activity, and DPPH radical scavenging capacity calculated using entropy weight method, the extraction conditions were optimized for solvent ratio, liquid-to-solid ratio, extraction time, and particle size. The inhibitory effects of BST on tyrosinase activity and melanin were assessed in α‑MSH-treated B16F10 cells, and its effect on reactive oxygen species (ROS) production was evaluated in H₂O₂-treated HaCaT cells. In a mouse model of melanogenesis induced by UVB radiation, the effect of BST gavage (100, 150, and 200 mg/kg) were evaluated by assessing skin conditions of the mice, Fontana-Masson staining, and detecting serum levels of cytokines related to melanogenesis, melanosome transport, metabolism, and inflammation. RESULTS: The optimized parameters for BST extraction included 50% ethanol, liquid-to-solid ratio of 15:1, extraction time of 1 h, and 20-mesh particle size. BST exhibited strong free radical-scavenging activity and significantly reduced melanogenesis and increased tyrosinase protein in B16 cells, and lowered ROS production in HaCaT cells. In the mouse models of melanogenesis, BST significantly suppressed the melanogenic enzymes and inflammatory responses by reducing the levels of tyrosinase and TNF-α, thereby effectively reversed UVB-induced photoaging and hyperpigmentation. CONCLUSIONS: The optimized BST extraction process is stable and predictable. BST shows good skin-whitening effect, which is mediated possibly by inhibiting tyrosinase activity and modulating oxidative stress and inflammatory pathways.
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