非瑟酮对LTA诱导小鼠子宫内膜炎症反应的影响

Effect of Fisetin on LTA-induced endometrial inflammation in mice

为探究非瑟酮(Fisetin)对金黄色葡萄球菌脂磷壁酸(lipid teichoic acid,LTA)诱导的子宫内膜炎症反应的影响,试验选取20只8~10周龄的健康雌性昆明小鼠,随机分为4组,每组5只,包括对照组、LTA模型组、LTA+Fisetin(25 mg/kg)组、LTA+Fisetin(50 mg/kg)组。H&E染色法检测子宫组织病理变化,RT-qPCR和Western blot方法检测相关炎症细胞因子及TLR2介导的NF-κB信号通路的表达情况。结果表明,与对照组相比,LTA造模组的子宫明显肿胀;TNF-α、IL-1βmRNA表达量和蛋白表达量极显著升高;NF-κB p65和IκBα蛋白的磷酸化极显著增加。与LTA模型组相比,LTA+Fisetin(25 mg/kg)组和LTA+Fisetin(50 mg/kg)的子宫损伤得到缓解;TNF-α、IL-1β蛋白表达极显著降低,mRNA表达在Fisetin剂量为50 mg/kg时显著降低;TLR2介导的NF-κB信号通路中p65、IκBα蛋白的磷酸化水平极显著降低。综上所述,Fisetin通过抑制TLR2介导的NF-κB信号通路的激活减少炎症细胞因子的表达,从而对子宫内膜炎起到一定的治疗作用。

To investigate the effect of Fisetin on endometrial inflammation induced by staphylococcus aureus Lipid teichoic acid(LTA),twenty healthy female kunming mice aged 8-10 weeks were randomly divided into 4 groups with 5 mice in each group,including control group,LTA model group and LTA+Fisetin(25 mg/kg)group,LTA+Fisetin(50 mg/kg)group.H&E staining was used to detect the pathological changes of uterine tissues.The expression of inflammatory cytokines and TLR2-mediated NF-κB signaling pathway were detected by RT-qPCR and Western blot.The results showed that compared with the control group,the uterus in LTA model group was significantly swollen.TNF-αand IL-1βmRNA expression and protein expression were extremely significant increased.The phosphorylation of NF-κB p65 and IκBαwas extremely significant increased.Compared with LTA model group,LTA+Fisetin(25 mg/kg)group and LTA+Fisetin(50 mg/kg)group showed remission of uterine injury.TNF-αand IL-1βprotein expression was extremely significant decreased,and mRNA expression was significantly decreased when Fisetin concentration was 50 mg/kg.TLR2-mediated phosphorylation of p65 and IκBαin NF-κB signaling pathway was extremely significant reduced.In conclusion,Fisetin plays a therapeutic role in endometritis by inhibiting the activation of TLR2-mediated NF-κB signaling pathway by reducing the expression of inflammatory cytokines.