【摘要】 目的:探讨过氧化物酶体增殖物激活受体γ(RRAR-γ)激动剂罗格列酮干预Toll样受体4/磷脂酰肌醇3-激酶(TLR4/PI3K)信号通路对脂多糖(LPS)诱导人冠状动脉血管内皮细胞(HCAEC)缝隙连接蛋白43(Cx43)表达的影响。方法:用LPS诱导建立HCAEC炎症模型,将细胞分为模型组、TLR4激动剂KLA组、PI3K抑制剂LY294002组、罗格列酮组、KLA+罗格列酮组、LY294002+罗格列酮组,另设空白组(不作任何处理)。分别采用实时荧光定量PCR(qPCR)、Western blotting法检测细胞中Cx43、TLR4、PI3K m RNA和蛋白表达。结果:KLA+罗格列酮组TLR4表达明显低于KLA组(P<0.05)。LY294002+罗格列酮组PI3K表达明显低于LY294002组(P<0.05)。模型组Cx43表达明显低于空白组(P<0.05),KLA+罗格列酮组Cx43表达明显高于KLA组(P<0.05),LY294002+罗格列酮组Cx43表达明显高于LY294002组(P<0.05)。结论:PPAR-γ激动剂罗格列酮可抑制TLR4/PI3K信号通路并上调HCAEC中Cx43的表达。更多还原

【Abstract】 Objective: To explore the effect of peroxisome proliferator-activated receptor γ(PPAR-γ) activator rosiglitazone on connexin 43(Cx43) expression in LPS-induced human coronary artery endothelial cells(HCAEC) by the regulation of Toll-like receptor 4/phosphatidylinositol 3-kinase(TLR4/PI3 K) signaling pathway.Methods:HCAEC inflammation model was induced by LPS, and the cells were divided into model group, TLR4 agonist KLA group, PI3 K inhibitor LY294002 group, rosiglitazone group, KLA + rosiglitazone group, andLY294002+rosiglitazone group. The cells without any treatment served as a blank group.The mRNA and protein expression of CX43, TLR4 and PI3 K were detected by real-time fluorescence quantitative PCR(qPCR) and western blotting, respectively. Results:The expression of TLR4 in KLA+rosiglitazone group was lower than that in KLA group(P<0.05). The expression of PI3 K in LY294002 + rosiglitazone group was lower than that in LY294002 group(P<0.05). The expression of Cx43 in the model group was significantly lower than that in blank group(P<0.05). The expression of CX43 in KLA+rosiglitazone group was significantly higher than that in KLA group(P<0.05).The expression of Cx43 in the LY294002+rosiglitazone group was higher than that in the LY294002 group(P<0.05).Conclusion:PPAR-γ activator rosiglitazone can inhibit the TLR4/PI3 K signaling pathway and upregulate the expression of Cx43 in HCAEC.更多还原