【摘要】 目的:探讨盐酸法舒地尔(HF)对脂多糖(LPS)诱导人冠脉内皮细胞(HCAEC)中缝隙连接蛋白43(Cx43)表达的影响。方法:用不同浓度的LPS(0.01 mg/L、0.1 mg/L、1 mg/L、10 mg/L)及不同浓度的HF(10μmol/L、30μmol/L、50μmol/L、80μmol/L)分别刺激HCAEC,采用MTT法检测细胞活力。将HCAEC随机分为空白对照组、LPS组、HF组和LPS+HF组,分别采用Western blotting和免疫组化法检测HCAEC Cx43蛋白的表达。结果:LPS浓度≥1mg/L时,HCAEC活力显著降低(P<0.05);HF浓度≥50μmol/L时,HCAEC活力显著降低(P<0.05)。与空白对照组相比,LPS组HCAEC Cx43蛋白表达上调(P<0.05),HF组HCAEC Cx43蛋白表达下调(P<0.05);LPS预处理细胞1h后与HF共培养,与LPS组相比,LPS+HF组HCAEC中Cx43的表达下调(P<0.05)。结论:HF能抑制LPS诱导的HCAEC中Cx43蛋白表达的增加,保护内皮间缝隙连接,从而发挥抗动脉粥样硬化的作用。更多还原

【Abstract】 Objective:To evaluate the role of hydroxyfasudil(HF)in lipopolysaccharide(LPS)-mediated connexin 43(Cx43)expression in human coronary endothelial cells(HCAEC).Methods:HCAEC were exposed to five different concentrations of LPS(0mg/L,0.01mg/L,0.1mg/L,1mg/L and 10mg/L)and HF(0μmol/L,10μmol/L,30μmol/L,50μmol/L and 80μmol/L)respectively,followed by MTT assay to test cell viability.HCAEC were randomly divided into the control group,LPS group,HF group and LPS+HF group.Cx43 expression was detected by western blotting and immunohistochemistry in HCAEC after24 htreatment.Results:The viability of HCAEC was significantly inhibited when the concentration of LPS was increased to 1mg/L(P <0.05)or the concentration of HF was increased to 50μmol/L(P <0.05).Compared with the control group,the expression of Cx43 was up-regulated in the LPS group(P <0.05),while it was down-regulated in the HF group(P <0.05).Furthermore,the expression of Cx43 was significantly down-regulated when co-treatment with LPS and HF(P <0.05).Conclusion:HF exerts an effect of anti-atherosclerosis by suppressing LPS-induced Cx43 expression in HCAEC and enhancing formation of endothelial gap junctions.更多还原