Nan Fang Yi Ke Da Xue Xue Bao = Journal Of Southern Medical University[JOURNAL]
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200 papers
[cGAS-STING agonist cGAMP enhances natural killer cell-mediated cytotoxicity against gastric cancer cells].
Wang Q, Chai Z, Deng Y … +4 more , Zhang Z, Gong Y, Gao S, Feng P
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633700 · Full text
OBJECTIVES: To explore the molecular mechanism by which cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) agonists enhance cytotoxicity of natural killer (NK) cells against gastric cancer cells. METHODS...
OBJECTIVES: To explore the molecular mechanism by which cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) agonists enhance cytotoxicity of natural killer (NK) cells against gastric cancer cells. METHODS: NK-92 cells were cultured in X-VIVO15 medium to a density of 1×10⁶/mL and treated with 5, 1, or 0.2 μmol/L cGAMP for 24 h before co-culture with gastric cancer MGC-803 and MKN-45 cells in RPMI 1640 medium. The expression of IFN-γ in co-cultured NK-92 cells and tumor cells was detected by qPCR and ELISA. The treated NK-92 cells were then co-cultured with the tumor cells labeled with CellTracker™ CM-DiI at different ratios (1:1, 2:1, and 4:1), and tumor cell viability and cytotoxicity of NK-92 cells were determined using a dead cell staining kit and flow cytometry-based cytotoxicity assay. RESULTS: The cGAS-STING agonist cGAMP dose-dependently enhanced mRNA expression and secretion of the pro-inflammatory cytokines (such as IFN-γ and TNF-α) in NK-92 cells, and NK-92 cells treated with 5 μmol/L cGAMP showed approximately 3-fold increase of IFN-γ and TNF-α levels. cGAMP treatment also upregulated the expression of activating receptors (such as NKp36 and NKp44) on the cell surface and activated the STING-TBK1-IRF3 signaling pathway in NK-92 cells. NK-92 cells pretreated with cGAMP showed increased cytotoxicity against MGC-803 and MKN-45 cells, which could be reversed by treatment with H-151 (a STING inhibitor). In tumor-bearing nude mice, combined treatment with cGAMP and NK cells reduced the mass of xenografts by nearly 40% and significantly slowed tumor growth. CONCLUSIONS: Activating the cGAS-STING pathway can enhance IFN-γ secretion of NK cells to improve their cytotoxicity against gastric cancer cells, suggesting a therapeutic strategy for gastric cancer using NK cells combined with STING agonists.
[Verbenalin ameliorates intestinal inflammation and colitis in a mouse model of Crohn's disease by inhibiting the PI3K-AKT pathway].
Huang L, Zheng W, Hu J … +6 more , Song X, Tao L, Geng Z, Li J, Zuo L, Ge S
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633699 · Full text
OBJECTIVES: To investigate the therapeutic effect of verbenalin (VE) on Crohn's disease (CD)‑like colitis and the underlying molecular mechanism. METHODS: Fifty C57BL/6 mice were randomly divided into control group, TNBS...
OBJECTIVES: To investigate the therapeutic effect of verbenalin (VE) on Crohn's disease (CD)‑like colitis and the underlying molecular mechanism. METHODS: Fifty C57BL/6 mice were randomly divided into control group, TNBS group, and low-, medium-, and high-dose VE treatment groups (10). Mouse models of CD-like colitis were established in all but the control group by enema with 25 mg/L TNBS dissolved in ethanol, and the mice in VE treatment groups received daily intraperitoneal injections of VE at 5, 10, or 20 mg/kg for 7 days. Cultured colon organoids derived from mouse crypts were exposed to 100 μg/mL lipopolysaccharide (LPS) for 24 h and treated with 5, 10, or 20 μmol/L VE. The therapeutic effects of VE in the mouse models were evaluated by assessing changes in disease activity index (DAI), histopathological scores, and spleen index. In both colonic mucosa of the mouse models and the colon organoids, the levels of inflammatory cytokines, expressions of tight junction proteins, and changes in PI3K-AKT pathway proteins were analyzed, and the regulatory mechanism of VE was verified using the PI3K-AKT agonist 740 Y-P. RESULTS: In TNBS-treated mice, VE treatment significantly reduced DAI, histopathological scores, and spleen index, and mitigated weight loss, colon shortening and bacterial translocation. VE obviously lowered the expression of pro-inflammatory cytokines in colonic mucosa of the mice and the colon organoids, upregulated ZO-1 and claudin-1 expressions, and reduced bacterial translocation. VE significantly downregulated p-PI3K and p-AKT protein expressions, which was reversed by treatment with 740 Y-P. CONCLUSIONS: VE inhibits intestinal inflammation and protects intestinal barrier function in mice with CD-like colitis by modulating the PI3K-AKT signaling pathway.
[ Injection in synergy with linezolid alleviates inflammatory injury in mice with MRSA pneumonia by inhibiting the Hla-NLRP3 pathway].
Yin M, Li R, Yang K … +2 more , Jiao W, Liu X
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633698 · Full text
OBJECTIVES: To evaluate the synergistic protective effect of linezolid (LZD) combined with Injection (XBJ, a traditional Chinese medicine injection) against pneumonia caused by methicillin-resistant (MRSA) in mice and...
OBJECTIVES: To evaluate the synergistic protective effect of linezolid (LZD) combined with Injection (XBJ, a traditional Chinese medicine injection) against pneumonia caused by methicillin-resistant (MRSA) in mice and explore the underlying mechanism. METHODS: Fifty C57BL/6J mice with pneumonia induced by tracheal instillation of MRSA were randomized equally into model group, low- and high-dose XBJ treatment groups (13 and 80 mg·kg·d, respectively), and combined treatment groups with low- and high-dose XBJ (6.5 and 13 mL·kg·d, respectively) and LZD (80 mg·kg ·d), with 10 PBS-treated mice as the normal control group. The minimum inhibitory concentration (MIC) of XBJ and LZD against MRSA and their effects on bacterial growth and hemolytic activity were assessed . After the treatments, lung pathologies of the mice were observed withHE staining, and IL-6, TNF-α, IL-1β, and IL-18 levels in lung homogenate were measured using ELISA; the mRNA and protein expressions of Hla, NLRP3, caspase-1, and ASC were detected using qPCR and Western blotting, and pulmonary expressions of NLRP3, caspase-1, and ASC were examined with immunohistochemistry. RESULTS: The combined treatment with LZD and XBJ significantly improved survival rates of the mouse models, reduced inflammatory cell infiltration and lung injury scores, decreased the levels of IL-6, TNF-α, IL-1β, and IL-18, and downregulated mRNA and protein expressions of Hla, NLRP3, caspase-1, and ASC. XBJ alone showed no antibacterial activity against MRSA but inhibited α-hemolysin (Hla) secretion both and to suppress NLRP3-mediated inflammation, while LZD did not produce this effect. CONCLUSIONS: LZD combined with XBJ produces enhanced efficacy for improving MRSA pneumonia possibly due to XBJ-induced inhibition of NLRP3-mediated inflammatory response via inhibiting α-hemolysin secretion.
[Veratric acid relieves oxidative stress and DSS-induced colitis in mice by activating the Nrf2/HO-1 signaling pathway].
Yin L, Zhang K, Qiao T … +6 more , Niu M, Yin L, Liu X, Geng Z, Li J, Hu J
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633697 · Full text
OBJECTIVES: To investigate the molecular mechanism by which veratric acid (VA) ameliorates oxidative stress injury and intestinal barrier dysfunction in mice with dextran sulfate sodium (DSS)-induced colitis. METHODS: Th...
OBJECTIVES: To investigate the molecular mechanism by which veratric acid (VA) ameliorates oxidative stress injury and intestinal barrier dysfunction in mice with dextran sulfate sodium (DSS)-induced colitis. METHODS: Thirty male C57BL/6 mice were randomized equally into control group, DSS model group, and VA treatment group. The mice were assessed for changes in body weight, disease activity index (DAI), colon length, and colonic histopathology. Colonic expressions of TNF-α, IL-6, and IL-10 and oxidative stress markers (SOD, GSH, MDA, and COX-2) were determined using ELISA, and the expressions of tight junction proteins (ZO-1 and claudin-1) and Nrf2/HO-1 pathway proteins were detected using immunofluorescence staining and Western blotting. In Caco-2 cells with H₂O₂-induced oxidative stress, ROS accumulation was examined using flow cytometry and a DCFH-DA probe, and Nrf2 inhibitor (ML385) was used to validate the mechanism of VA for ameliorating oxidative stress. RESULTS: VA treatment significantly alleviated DSS-induced body weight loss, colon shortening and the increase of DAI score of the mice, resulting also in improved crypt structure and increased expressions of ZO-1 and claudin-1 and the number of goblet cells. VA obviously reduced colonic levels of TNF‑α and IL-6, increased the level of IL-10, and reversed DSS-induced decreases in SOD and GSH activity and increases in MDA and COX-2 levels. In H₂O₂-treated Caco-2 cells, VA decreased ROS-positive cell rate and intracellular ROS accumulation, and increased cellular expressions of claudin-1 and ZO-1. Mechanistically, VA promoted the expressions of Nrf2 and the downstream HO-1 protein, and ML385 partially reversed ROS-reducing effect of VA. CONCLUSIONS: VA enhances antioxidant defense, inhibits inflammation, and repairs intestinal barrier function in mice with DSS-induced colitis by activating the Nrf2/HO-1 pathway, suggesting a novel strategy for treatment of inflammatory bowel disease.
[High expression of MPP6 predicts poor patient prognosis and promotes malignant biological behaviors of hepatocellular carcinoma cells].
Yu H, Shao Y, Cheng Q … +3 more , Zhou X, Geng H, Yang Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633696 · Full text
OBJECTIVES: To investigate the expression of membrane protein palmitoylated 6 (MPP6) in hepatocellular carcinoma (HCC) and analyze its correlation with clinicopathological features and patient prognosis and its impact on...
OBJECTIVES: To investigate the expression of membrane protein palmitoylated 6 (MPP6) in hepatocellular carcinoma (HCC) and analyze its correlation with clinicopathological features and patient prognosis and its impact on biological behaviors of HCC cells. METHODS: We examined MPP6 expressions using immunohistochemistry in tumor and adjacent tissues from 118 HCC patients undergoing surgeries in our hospital from January, 2017 to December, 2019, and analyzed the correlation of MPP6 expression levels with clinicopathological data and overall survival (OS) of the patients using Cox regression analysis. In human hepatoma Hep3B cells, the effects of lentivirus-mediated MPP6 knockdown on biological behaviors of the cells were evaluated using colony formation assay, wound-healing assay, Transwell assay and flow cytometry. RESULTS: Compared with adjacent tissues, HCC tissues showed significant overexpression of MPP6 (<0.001), whose expression levels was correlated with liver cirrhosis (=0.028) and baseline albumin level (=0.035) of the patients. Survival analysis suggested that HCC patients with a high expression of MPP6 had a worse prognosis (<0.001); Cox regression analysis indicated that MPP6 expression (=0.012, HR: 2.335, 95% : 1.502-3.629) was an independent predictor of OS of HCC patients following hepatectomy. In Hep3B cells, MPP6 knockdown obviously inhibited cell proliferation, migration and invasion (<0.05) and caused cell cycle arrest in G0/G1 phase (<0.001). CONCLUSIONS: MPP6 is highly expressed in HCC tissues and correlates with important clinicopathological features and unfavorable prognosis of the patients. MPP6 knockdown inhibits proliferation, migration and invasion and blocks cell cycle progression in G0/G1 phase.
[Allergens induce activation of blood CCR3 granulocyte subsets in patients with perennial allergic rhinitis].
Wang Q, Xu W, Gu F … +3 more , Wang S, He S, Wang J
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633695 · Full text
OBJECTIVES: To explore the effects of allergens on activation of blood CCR3 granulocyte subtypes in patients with allergic rhinitis (AR). METHODS: Flow cytometry was used to examine the effects of allergens on CD63 and C...
OBJECTIVES: To explore the effects of allergens on activation of blood CCR3 granulocyte subtypes in patients with allergic rhinitis (AR). METHODS: Flow cytometry was used to examine the effects of allergens on CD63 and CD203c expressions on CCR3CD203c eosinophils and CCR3CD203c basophils of AR patients. Plasma levels of IL-25 and TSLP of the patients were detected with multiplex immunoassay and ELISA, respectively, and their correlations with eosinophils and basophils were analyzed. RNA-sequencing of blood CD16 granulocytes from AR patients was performed, and enrichment analysis was used to explore the functions and potential mechanisms of the differentially expressed genes. RESULTS: The percentages of eosinophils and basophils in CCR3 granulocytes increased significantly in AR patients (<0.005), and exposure to allergens further upregulated the percentage of basophils (<0.005). CD63 expression was significantly increased in patients with seasonal AR (sAR) and perennial AR (pAR) (<0.005) but not in AR patients negative for skin prick test (nAR). Allergen exposures enhanced the expressions of CD63 and CD203c on eosinophils and basophils in pAR patients (<0.005). Elevated plasma IL-25 and TSLP levels in AR patients were associated with increased eosinophil and basophil counts (<0.005). The 3999 differentially expressed genes in CD16 granulocytes from AR patients positive for skin prick test (SPT) were involved in protein synthesis, energy metabolism and immune function and in endocytosis, phagosome and carbon metabolism pathways. CONCLUSIONS: The findings in this study enrich the understanding of the roles of CCR3 eosinophils and basophils in the pathogenesis of SPTAR and reveal potential therapeutic targets for AR.
[Quercetin inhibits proliferation and migration and promotes apoptosis of gastric cancer cells by promoting phosphorylation-mediated YAP inactivation].
Wang Y, Wang W, Cheng S … +6 more , Feng Y, Zhang Z, Shi Q, Li Y, Hu Q, Wu M
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633694 · Full text
OBJECTIVES: To explore the molecular mechanisms by which quercetin regulates proliferation, migration, and apoptosis of gastric cancer cells. METHODS: Bioinformatics analysis was conducted to examine the differential exp...
OBJECTIVES: To explore the molecular mechanisms by which quercetin regulates proliferation, migration, and apoptosis of gastric cancer cells. METHODS: Bioinformatics analysis was conducted to examine the differential expression of Hippo pathway protein yes-associated protein (YAP) between gastric cancer and normal tissues and its correlation with patient survival rates. CCK-8 assay was used to evaluate the effect of quercetin on viability of gastric cancer HGC-27 cells. The expression levels of YAP and phosphorylated YAP (p-YAP) in gastric cancer and normal gastric tissues were detected using Western blotting. In HGC-27 cells with YAP knockdown, the effects of quercetin treatment on cell proliferation, migration and apoptosis were assessed using EdU assay, colony formation assay, Transwell assay, and flow cytometry; the localization of YAP was determined using immunofluorescence staining. Rescue experiments were performed by overexpressing YAP in HGC-27 cells. RESULTS: YAP expression was markedly lower in gastric cancer tissues than in normal tissues, and its expression level was negatively correlated with patient survival rates. Quercetin significantly inhibited the survival of HGC-27 cells, promoted MST1 and LATS1 expression, and activated the Hippo signaling pathway, leading to phosphorylation-mediated inactivation of YAP, thereby reducing its nuclear translocation. Both YAP knockdown and quercetin treatment significantly suppressed proliferation and migration and promoted apoptosis of HGC-27 cells. Overexpression of YAP substantially attenuated the inhibitory effects of quercetin in HGC-27 cells. CONCLUSIONS: Quercetin inhibits proliferation and migration and promotes apoptosis of gastric cancer cells by promoting phosphorylation-mediated inactivation of YAP.
[Cajanonic acid A derivative XJ-60 improves liver fibrosis in mice with non-alcoholic fatty liver disease by inhibiting the SP1/TGF-β/Smad3 signaling axis].
Geng Z, Hu L, Dai Y … +6 more , Luo R, Xu T, Liao X, Yuan Z, Wang J, Xiao Y
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633693 · Full text
OBJECTIVES: To investigate the mechanism of XJ-60, a derivative of cajanonic acid A, for alleviating liver fibrosis in mice with non-alcoholic fatty liver disease (NAFLD). METHODS: Twelve mice were randomized equally in...
OBJECTIVES: To investigate the mechanism of XJ-60, a derivative of cajanonic acid A, for alleviating liver fibrosis in mice with non-alcoholic fatty liver disease (NAFLD). METHODS: Twelve mice were randomized equally into NAFLD model group and XJ-60 treatment group with daily gavage of 50 mg/kg XJ-60, with 6 mice serving as the control group. Successful modeling of NAFLD was validated using HE and Oil Red O staining and by measuring ALT and AST levels of the mice. Immunohistochemistry was used for detecting hepatic expressions of specific protein 1 (SP1) and fibronectin (FN); the changes in hepatic expressions of epithelial-mesenchymal transition (EMT) markers, extracellular matrix (ECM) markers, and IL-6 were detected using Western blotting and ELISA. In AML12 cells induced with free fatty acids (FFA), the effect of XJ-60 on expressions of SP1, transforming growth factor-β (TGF-β), Smad3/-Smad3, and the markers of EMT and ECM were analyzed. SP1 knockdown experiment was performed to validate the role of TGF‑β/Smad3 signaling axis in NAFLD. RESULTS: XJ-60 treatment significantly reduced serum lipid levels, improved liver histology, and lowered hepatic IL-6 expression in mice. The expression level of SP1 was positively correlated with α-SMA and negatively with E-ca expression. In AML12 cells, XJ-60 treatment at 10 μmol/L significantly reduced FFA-induced lipid accumulation and downregulated cellular expressions of SP1, TGF-β, -Smad3, and the EMT and ECM markers; SP1 knockdown obviously inhibited the expression levels of TGF-β, Smad3 and ECM markers. CONCLUSIONS: XJ-60 ameliorates liver fibrosis and steatosis in mice with NAFLD possibly through SP1-mediated inhibition of the TGF‑β/Smad3 pathway to reduce ECM deposition.
[Dual role of tea consumption in gastrointestinal disease risks: analysis using a risk prediction model integrating interpretable machine learning and large language model].
Chen J, Chen Z, Lin Z … +5 more , Fang M, Shen C, Xu Q, Zhang X, Lu L
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633692 · Full text
OBJECTIVES: To explore the correlation of tea consumption with risks of gastrointestinal diseases using a risk prediction model integrating interpretable machine learning and a large language model. METHODS: A survey was...
OBJECTIVES: To explore the correlation of tea consumption with risks of gastrointestinal diseases using a risk prediction model integrating interpretable machine learning and a large language model. METHODS: A survey was conducted among the patients undergoing both gastroscopy and 13C-urea breath testing at Gastrointestinal Endoscopy Center of Anxi Hospital of Traditional Chinese Medicine. Univariate analysis was performed to determine the suitability of feature selection. The collected data were randomly divided into training and testing sets in a 7:3 ratio. Support Vector Machine (SVM), K-Nearest Neighbors (KNN), Logistic Regression (LR), Random Forest (RF), Extreme Gradient Boosting (XGB), and Deep Neural Network (DNN) were applied to identify the best classifier for predicting high-risk gastrointestinal conditions. Bayesian optimization algorithm was used to obtain the optimal hyperparameter combinations for the 6 models. After Model fitting, the interpretability of the best models was analyzed using SHapley Additive exPlanations (SHAP). The DeepSeek-R1 base language model was fine-tuned with gastrointestinal disease dataset and Chinese medical online consultation data to obtain the final model. RESULTS: The study included 503 participants. All the selected features showed association with gastrointestinal diseases, but only age exhibited a significant linear correlation (β=0.023, SE=0.008, =2.942, =0.003). DNN model performed the best with a good accuracy (0.68), precision (0.68), recall rate (0.85), F1 Score (0.75), and AUC (0.74). The top 3 important features were age, DOB value, and smoking history. The large language model constructed provided recommendations consistent with those of professional physicians based on gastroscopy results. CONCLUSIONS: DNN model is effective for predicting gastrointestinal disease risk and offers reliable support for clinical risk assessment and decision-making regarding endoscopy. Smoking cessation, moderate alcohol consumption, and reasonable tea intake may help prevent gastrointestinal diseases.
[Establishment of an Epstein-Barr virus infection model using human nasal organoids].
Wei J, Zheng H, Zhao Y … +3 more , Yu Y, Xu Y, Li G
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633691 · Full text
OBJECTIVES: To develop an cost-effective and convenient method for culturing human nasal organoids to establish an Epstein-Barr virus (EBV) infection model. METHODS: Nasal polyp tissue obtained from surgery was routinel...
OBJECTIVES: To develop an cost-effective and convenient method for culturing human nasal organoids to establish an Epstein-Barr virus (EBV) infection model. METHODS: Nasal polyp tissue obtained from surgery was routinely washed, cut, digested and filtered to obtain cell clusters. The cell clusters were then expanded into undifferentiated nasal organoids through dynamic suspension culture under matrix-free conditions, followed by a 14-day differentiation induction treatment to obtain differentiated nasal organoids. The major cellular components of the organoids were identified by immunofluorescence staining and immunohistochemistry. The nasal organoids were infected by EBV , and viral replication was verified by detecting the expressions of the virus-specific genes EBNA1 and BALF5 using RT-qPCR and immunofluorescence staining. RESULTS: Nasal organoids consisting of basal cells, mucous cells, and ciliated cells in a martigel-free system were obtained successfully by dynamic suspension culture. The differentiated nasal organoids expressed high levels of EBV-associated receptors EphA2, NRP1, and NMHCII-A. Both the undifferentiated and differentiated nasal organoids could be infected by EBV. Viral replication in the organoids increased with the viral exposure load, and the differentiated organoids appeared more permissive to viral replication. CONCLUSIONS: The matrigel-free dynamic suspension culture method is economical and simple for constructing nasal organoids, which can be used as a model of EBV infection for studies of epithelial EBV infection.
[ Recipe improves ulcerative colitis in rats by regulating Th17/Treg immune balance].
Li B, Zhou X, Lang X … +2 more , Kang X, Liu J
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633690 · Full text
OBJECTIVES: To explore the mechanism of Recipe (XZJD) for improving ulcerative colitis (UC). METHODS: SD rat models of UC were randomized into 5 groups (=10) for daily gavage with saline, mesalamine, or low-, medium- or...
OBJECTIVES: To explore the mechanism of Recipe (XZJD) for improving ulcerative colitis (UC). METHODS: SD rat models of UC were randomized into 5 groups (=10) for daily gavage with saline, mesalamine, or low-, medium- or high-dose XZJD for 14 days, with 10 normal rats with saline gavage as the control group. Pathological changes in the colon of the rats were observed using HE staining, and serum IL-6, IL-10 and IL-17 levels and their expressions in the colon tissues were determined with ELISA and immunohistochemistry. The expressions of occludin and ZO-1 and percentages of Th17 and Treg cells in the colon tissues were detected using immunofluorescence staining and flow cytometry; the mRNA and protein expressions of ROR-γt and Foxp3 were detected with RT-PCR and Western blotting. RESULTS: The rat models of UC showed obvious colonic mucosal damage with massive inflammatory cell infiltration, increased IL-6 and IL-17 levels and lowered IL-10 level in both the serum and colonic tissues, reduced expression levels of occludin and ZO-1, increased Th17 and lowered Treg cell percentages, increased RORγt mRNA and protein expressions, and reduced Foxp3 mRNA and protein expressions in the colonic tissue. Treatment with XZJD significantly alleviated inflammatory response in the colonic mucosa and effectively reversed the changes in IL-6, IL-17 and IL-10 levels, expressions of occludin and ZO-1, percentages of Th17 and Treg cells, and the expressions of RORγt and Foxp3 in the colonic tissues of UC rats. CONCLUSIONS: XZJD can alleviate pathologies in the colonic mucosa in UC rats possibly by regulating Th17/Treg immune balance.
[Curcumin improves osteoporosis in type 2 diabetic mice by inhibiting RANBP3L expression].
Zou X, Zhang X, Li P … +2 more , Tian R, Lu X
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633689 · Full text
OBJECTIVES: To investigate the therapeutic mechanism of curcumin for osteoporosis induced by type 2 diabetes mellitus (T2DM). METHODS: In cultured MC3T3-E1 osteoblasts exposed to high glucose (HG), the effects of curcumi...
OBJECTIVES: To investigate the therapeutic mechanism of curcumin for osteoporosis induced by type 2 diabetes mellitus (T2DM). METHODS: In cultured MC3T3-E1 osteoblasts exposed to high glucose (HG), the effects of curcumin treatment on osteogenic differentiation and mineralization were examined by assessing alkaline phosphatase (ALP) activity and using alizarin red S (ARS) staining. RNA-seq sequencing was used to analyze the transcriptional characteristics of MC3T3-E1 osteoblasts in HG culture after curcumin treatment. In a mouse model of T2DM established by high-fat diet feeding and streptococcal injection, the effects of solvent vehicle, vehicle+RANBP3L knockdown, and RANBP3L knockdown+curcumin treatment on blood lipids, bone microstructure and calcium deposition was evaluated using ELISA, HE staining, and Alizarin red S staining. Osteogenic differentiation ability of mouse femoral tissues were assessed by detecting ALP, RANBP3L, OCN and RANKL expressions using immunohistochemical staining, RT-qPCR and Western blotting, and the changes in the TNF‑α/ NF‑κB pathway were detected with Western blotting. RESULTS: Curcumin obviously promoted proliferation and osteogenic differentiation of MC3T3-E1 cells in HG culture and down-regulated cellular expression of RANBP3L protein. In the diabetic mouse models, RANBP3L knockdown significantly improved bone microstructure and blood lipid balance, increased expression levels of osteogenic markers, decreased blood glucose level, and caused inhibition of the TNF‑α/NF‑κB signaling pathway. The combined treatment with curcumin further reduced RANBP3L expression levels in the bone tissue and significantly enhanced the therapeutic effect. CONCLUSIONS: Curcumin promotes osteogenesis, alleviates glucose and lipid metabolism disorders, and improves osteoporosis in type 2 diabetic mice possibly by inhibiting TNF‑α/NF‑κB signaling pathway suppressing RANBP3L expression.
[Isovitexin alleviates myocardial oxidative stress injury in diabetic mice by enhancing myocardial SIRT3 expression and reducing oxidative stress].
Peng Y, Jiang Y, Ma D … +4 more , He A, Lü D, Luo M, Luo S
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633688 · Full text
OBJECTIVES: To investigate the protective effect of isovitexin (ISO) on the myocardium of diabetic mice and explore its mechanism. METHODS: Eighteen adult male C57 mice were randomly divided into control group, diabetes...
OBJECTIVES: To investigate the protective effect of isovitexin (ISO) on the myocardium of diabetic mice and explore its mechanism. METHODS: Eighteen adult male C57 mice were randomly divided into control group, diabetes mellitus (DM) group and DM+ISO group (=6). Primary cultures of neonatal mouse cardiomyocytes (NMCMs) were exposed to high glucose (33 mmol/L) and treated with ISO alone or in combination with 3-TYP (a SIRT3 inhibitor). HE staining was used to evaluate myocardial injury in the diabetic mice, and the levels of MDA, SOD and GSH-Px in the myocardium were detected with ELISA. The expressions of iNOS, NOX2 and 8-OHdG were detected using immunohistochemistry and fluorescence staining. Western blotting was used to analyze the expression levels of NRF2, NOX2, NQO1, and SIRT3, and ROS levels were determined with flow cytometry. RESULTS: The diabetic mice showed obvious inflammatory cell infiltration in the myocardium, increased myocardial levels of IL-1β, IL-6 and TNF‑α, decreased expression levels of NQO1, NRF2 and SIRT3 proteins, and increased expression levels of NOX2 and AC-SOD2 proteins. ISO treatment of the diabetic mice significantly reduced myocardial inflammatory cell infiltration, lowered the levels of IL-1β, IL-6 and TNF‑α, restored the protein levels of NQO1, NRF2 and SIRT3, and decreased the protein levels of NOX2 and AC-SOD2. CONCLUSIONS: ISO can alleviate diabetic myocardial injury in mice by promoting SIRT3 expression and reducing oxidative stress.
[Development of an LC-MS/MS method for 32 steroid hormones and exploration of their gestational variations].
Zhou Q, Chen J, Nie C … +3 more , Wang Q, Xia F, Zhou H
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633687 · Full text
OBJECTIVES: To establish a highly sensitive and specific liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based analytical method for detecting steroid hormones in human serum. METHODS: Solid-phase extraction (S...
OBJECTIVES: To establish a highly sensitive and specific liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based analytical method for detecting steroid hormones in human serum. METHODS: Solid-phase extraction (SPE) was used for sample pretreatment. Chromatographic conditions were optimized to achieve baseline separation, and mass spectrometry parameters were adjusted to ensure accurate detection of trace amounts of hormones. After validation of the linear range, accuracy, and precision, the method was applied in detection of serum samples from normal pregnant women for analyzing dynamic variation characteristics of 32 steroid hormones during the first, second, and third trimesters of pregnancy. RESULTS: The linear range of the method was 0.001-7500 ng/mL, with a limit of detection (LOD) of 0.0007 ng/mL. Both intra-day and inter-day coefficients of variation (CV) of the method were less than 10%, the spiked recovery ranged from 86.21% to 112.67%, the extraction efficiency was 85.05%-106.3%, and the matrix effects were 85.60%-113.22%. The results of detection using this method for serum steroid hormones during pregnancy revealed significant elevation of most of the hormones (such as 11-deoxycortisol, 11β-hydroxyprogesterone, dehydroepiandrosterone sulfate, and estriol) with the progression of pregnancy, indicating a close correlation with the development of fetal-placental function. Some hormones increased in the third trimester, possibly due to maternal adaptive regulation and maturation of fetal adrenal function. CONCLUSIONS: The detection results using the method established in this study reveal dynamic variations of steroid hormones during pregnancy, which provides clues for further physiological and pathological studies of these hormones.
[ Decoction promotes efferocytosis of interstitial Cajal cells in rats with slow transit constipation by inhibiting the PI3K/Akt signaling pathway].
Qiu J, Chen M, Man R … +4 more , Chen X, Qiu D, Chang Q, Ma H
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633686 · Full text
OBJECTIVES: To explore the mechanism of Decoction (HYTBD) for relieving slow transit constipation (STC) in rats. METHODS: Sixty SD rat models of STC induced by intragastric administration of loperamide hydrochloride sus...
OBJECTIVES: To explore the mechanism of Decoction (HYTBD) for relieving slow transit constipation (STC) in rats. METHODS: Sixty SD rat models of STC induced by intragastric administration of loperamide hydrochloride suspension were randomized equally into 5 groups for treatment with daily gavage with saline (STC model group), low-, medium-, or high-dose HYTBD, or mosapride (positive control group), with another 12 normal rats receiving saline gavage as the blank control group. The first black stool time, fecal water content and intestinal propulsion rate of the rats were measured, and the ultrastructure of interstitial Cajal cells (ICCs) was observed using transmission electron microscopy to calculate the mitochondrial vacuolar rate. The phagocytosis rate of macrophages was detected using immunofluorescence assay, and colonic pathologies were examined using HE staining. The colonic expression levels of c-Kit, CD47, PI3K and Akt were detected with immunohistochemistry or Western Blotting, and their correlations with efferocytosis were analyzed. RESULTS: The rat models of STC showed significant ultrastructural damage of the ICCs with increased first black stool time, mitochondrial vacuolar rate, and colonic expression levels of CD47, p-PI3K/PI3K and p-Akt/Akt proteins, lowered fecal water content, intestinal propulsion rate and c-Kit expression level, without significant changes in phagocytic rate. Treatment with HYTBD, especially at the high dose, significantly increased fecal water content, intestinal propulsion rate, phagocytosis rate and colonic c-Kit expression, and decreased the first black stool time, mitochondrial vacuolar rate, and colonic expressions of CD47, p-PI3K/PI3K and p-Akt/Akt in the mouse models. CONCLUSIONS: HYTBD improves STC in rats possibly by down-regulating colonic CD47 expression and improving macrophage phagocytosis rate via inhibiting PI3K and Akt phosphorylation, thereby promoting efferocytosis of the ICCs.
[Total Astragalus saponins reduce astrocyte swelling and AQP4 expression following oxygen-glucose deprivation and reoxygenation by inhibiting the p38 pathway].
Yin Q, Lei Y, Wang X … +2 more , Yang G, Tang Z
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633685 · Full text
OBJECTIVES: To investigate the effect of total Astragalus saponins (AST) on astrocyte swelling induced by glucose-oxygen deprivation and reoxygenation (OGD/R) and its molecular mechanism. METHODS: Primary astrocytes isol...
OBJECTIVES: To investigate the effect of total Astragalus saponins (AST) on astrocyte swelling induced by glucose-oxygen deprivation and reoxygenation (OGD/R) and its molecular mechanism. METHODS: Primary astrocytes isolated from the brain of post-natal day 2 SD rats were treated with solvent vehicle, AST, or AST combined with U-46619 (a p38 activator) 24 h prior to and during exposure to OGD/R. The changes in cell volume and morphology were observed, and intracellular reactive oxygen species (ROS) levels and lactate dehydrogenase (LDH) activity were detected. The expression of aquaporin 4 (AQP4) on cell membrane was observed using immunofluorescence confocal microscopy, and Western blotting was performed to detect the changes in p38 signaling pathway phosphorylation levels and AQP4 expression level. RESULTS: AST treatment significantly reduced OGD/R-induced increase in astrocyte volume, ROS levels and LDH release. The AST-treated cells also exhibited improved cell morphology, reduced aggregation of AQP4 on the cell membrane, and decreased p38 phosphorylation and AQP4 expression levels. The protective effects of AST against OGD/R-induced cell injuries were significantly attenuated by combined treatment of the cells with U-46619. CONCLUSIONS: AST alleviate astrocyte swelling induced by OGD/R injury by inhibiting the activation of the p38 signaling pathway and AQP4 overexpression on the cell membrane.
[Plasma metabolites mediates the causal effect of inflammatory proteins on Alzheimer's disease: a Mendelian randomization study].
Chen M, Huang R, Yang Z
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633684 · Full text
OBJECTIVES: To investigate the causal relationship between inflammatory proteins and Alzheimer's disease (AD) and the mediating role of plasma metabolites therein. METHODS: Using Mendelian mandomization (MR) methods and...
OBJECTIVES: To investigate the causal relationship between inflammatory proteins and Alzheimer's disease (AD) and the mediating role of plasma metabolites therein. METHODS: Using Mendelian mandomization (MR) methods and publicly available genome-wide association study (GWAS) data, we selected 91 single nucleotide polymorphisms (SNPs) that were strongly linked to inflammatory proteins without reverse causality with AD as the outcome. A bidirectional two-sample MR analysis was performed. Inflammatory proteins with causal links to AD were identified via inverse variance weighted (IVW) analysis. A mediation MR analysis was then performed using 1400 plasma metabolites to assess their mediating role in this causal pathway. RESULTS: The preliminary bidirectional MR analysis identified 3 inflammatory proteins that had a potential positive causal association with AD without reverse causality: Axin-1, C-X-C motif chemokine ligand 11 (CXCL11), and interleukin-12β (IL-12β). Elevated levels of Axin-1 were positively causally associated with AD risk (OR=1.082, 95% : 1.009-1.159; =0.026), while CXCL11 (OR=0.951, 95% : 0.914-0.990; =0.026) and IL-12β (OR=0.959, 95% : 0.926-0.994; =0.026) were negatively causally associated with AD risk. Sensitivity analyses indicated that these causal effects exhibited no heterogeneity or pleiotropy. In the mediation analysis, 18 plasma metabolites with causal links to AD were identified, among which 3 plasma metabolites exhibited mediating effects in the inflammatory protein-AD causal relationship. Methyl-4-hydroxybenzoate sulfate partially mediated the effect between Axin-1 and AD (20.10%). Pregnenetriol sulfate partially mediated the effect between CXCL11 and AD (18.20%). The ratio of spermidine to ornithine played an important mediating role between IL-12β and AD, with a mediating effect of 43.40%. CONCLUSIONS: This study reveals how specific inflammatory proteins influence AD risk via plasma metabolites and provides genetic evidence for inflammatory-metabolic interactions in AD to facilitate the identification of potential biomarkers and targets for early detection and intervention of AD.
[ alleviates lead exposure-induced learning and memory impairment in mice by regulating bile acid metabolism and inhibiting hippocampal NLRP3 expression].
Li L, Yu W, Tan M … +3 more , Li Y, Liu A, Meng X
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633683 · Full text
OBJECTIVES: To explore the mechanism of () for alleviating learning and memory impairments caused by lead exposure. METHODS: Twenty-four C57BL/6J mice were randomized equally into control group, lead exposure (100 mg/L)...
OBJECTIVES: To explore the mechanism of () for alleviating learning and memory impairments caused by lead exposure. METHODS: Twenty-four C57BL/6J mice were randomized equally into control group, lead exposure (100 mg/L) group, and treatment group with daily gavage of (10 CFU) for 10 weeks. Learning and memory abilities of the mice were evaluated using Morris water maze test, and blood lead level and bile acid levels were determined using inductively coupled plasma mass spectrometry (ICP-MS) and liquid chromatography-mass spectrometry (LC-MS), respectively. Hippocampal pathologies of the mice were examined with HE staining, and immunohistochemistry was used to observe morphological changes and microglia activation in the hippocampus. Serum levels of TNF‑α and IL-1β of the mice were determined with ELISA, and hippocampal expression levels of NLRP3 and TGR5 proteins were detected using Western blotting. RESULTS: Compared with those in lead exposure group, the mice receiving intervention showed significantly increased exploration time, swimming distance, and target platform crossings with reduced latency period to find the hidden platforms in Morris water maze test. intervention partially reversed lead exposure induced reduction of serum levels of deoxycholic acid, 3-hydroxydeoxycholic acid, 3-hydroxyursodeoxycholic acid, 3-thiodeoxycholic acid, and 3-thio‑α‑methylcholic acid. The treatment also significantly reduced hippocampus pathologies in mice with lead exposure, and reduced their serum levels of IL-1β and TNF‑α and hippocampal NLRP3 protein expression levels. CONCLUSIONS: can alleviate learning and memory impairments caused by lead exposure in mice possibly by regulating bile acid metabolism and inhibiting hippocampal expression of NLRP3 protein.
[ Formula inhibits proliferation, invasion and migration of nasopharyngeal carcinoma cells by inhibiting the AKT1/GLUT1 signaling pathway].
Xu H, He L, Xiong Y … +6 more , Zou F, Lin T, Jiang Z, Tang L, He Y, Zhou F
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633682 · Full text
METHODS: Molecular docking was employed to analyze the binding affinity between the active components of YQJDF and AKT1. MTT assay, real-time cell analysis (RTCA), wound healing assay and Matrigel invasion chamber assay...
METHODS: Molecular docking was employed to analyze the binding affinity between the active components of YQJDF and AKT1. MTT assay, real-time cell analysis (RTCA), wound healing assay and Matrigel invasion chamber assay were used to evaluate the effect of YQJDF extract on proliferation, migration and invasion abilities of human NPC cell lines 5-8F and 6-10B, and the changes in cellular protein expression levels were detected using Western blotting. In a BALB/c nude mouse model bearing NPC cell xenografts, tumor growth were observed following treatment with daily gavage with normal saline or YQJDF extract (15.357 g/kg) for 18 consecutive days or with intraperitoneal injections of 5-Fu every other day. The changes in the expressions of AKT1/GLUT1 signaling axis proteins in the xenografts were examined using Western blotting. RESULTS: In the NPC cell lines, treatment with YQJDF extract significantly inhibited cell proliferation, migration, and invasion, and downregulated the expressions of p-AKT, GLUT1, XIAP, N-cadherin, and vimentin. The application of GLUT1 or AKT1 activators partially reversed the inhibitory effects of YQJDF on the NPC cells. In the tumor-bearing mouse models, treatment with YQJDF extract obviously suppressed tumor growth and down-regulated the expression of AKT, p-AKT and GLUT1 in the tumor tissues. CONCLUSIONS: YQJDF inhibits proliferation, invasion, and migration of NPC cells by inhibiting the AKT1/GLUT1 signaling pathway.
[Radix codonopsis combined with Poria improves cognitive impairment in rats with unilateral common carotid artery ligation by regulating the ERα/PI3K/Akt signaling pathway].
Yang J, He Y, Guo Y … +5 more , Shang F, Hua L, Yang Y, Zhang X, Wei J
Nan Fang Yi Ke Da Xue Xue Bao · 2026 Feb · PMID 41633681 · Full text
OBJECTIVES: To investigate the mechanism of Radix codonopsis combined with Poria (CRP) for improving cognitive impairment induced by permanent unilateral common carotid artery ligation (UCCA) in rats. METHODS: UPLC-Q-TOF...
OBJECTIVES: To investigate the mechanism of Radix codonopsis combined with Poria (CRP) for improving cognitive impairment induced by permanent unilateral common carotid artery ligation (UCCA) in rats. METHODS: UPLC-Q-TOF-MS/MS and network pharmacology analysis were used to analyze the components of CRP in the blood and brain of rats medicated with CRP. Rat models of UCCA were treated with CRP gavage for 1 month, and Morris water maze, HE staining, and NeuN staining were used to assess the therapeutic efficacy. Metabolomics analysis, ELISA, immunohistochemistry, and Western blotting were employed to explore and validate the therapeutic mechanism of CRP. RESULTS: A total of 125 chemical constituents were identified in the brain tissue (89 Radix codonopsis components and 36 Poria components) and 126 in blood samples (85 Radix codonopsis components and 41 Poria components) of medicated rats. Network pharmacology analysis revealed that the therapeutic mechanism of CRP on dementia involved primarily the PI3K/Akt signaling pathway, regulated by the brain-targeting constituents of CRP. In UCCA rats, CRP treatment significantly improved their performance in Morris water maze test, alleviated neuronal damage in the hippocampus and cortex, and increased expression level of NeuN. Metabolomics analysis revealed significant enrichment of the estrogen and GABAergic synapse signaling pathways in CRP-treated rats. CRP obviously reduced the brain levels of glutamate and GABA/glutamate in UCCA rats, and downregulated the proteins expressions of ERα, p-PI3K/PI3K and p-Akt/Akt. CONCLUSIONS: CRP improves learning and memory impairment in UCCA rats possibly by modulating the ERα/PI3K/Akt signaling pathway in the brain.
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