摘要
目的:探讨左西孟旦对LPS诱导的乳鼠心肌细胞损伤的保护作用。方法:将原代培养的SD乳鼠的心肌细胞分为3组:对照组、模型组和左西孟旦干预组。模型组和左西孟旦干预组用10 mg/L的LPS处理6 h建模,其中左西孟旦干预组于造模前用终浓度为0.30μmol/L的左西孟旦预处理24 h。全自动生化仪检测3组细胞培养液LDH、CK含量;ELISA检测培养液TNF-α、IL-6含量;流式细胞仪检测细胞凋亡;Western blot检测凋亡相关蛋白Cleaved-Caspase-3及抗凋亡蛋白Bcl-2的表达。结果:与对照组比较,模型组细胞培养液中LDH、CK、TNF-α和IL-6含量增加,细胞凋亡率升高,凋亡蛋白Cleaved-Caspase-3表达增高,抗凋亡蛋白Bcl-2表达降低(P<0.05);与模型组比较,左西孟旦干预组细胞培养液中LDH、CK、TNF-α、IL-6含量减少,细胞凋亡率降低,Cleaved-Caspase-3表达量降低,Bcl-2表达增高(P<0.05)。结论:左西孟旦对LPS诱导的乳鼠心肌细胞损伤有保护作用,其机制可能与减少炎症因子释放,抑制Caspase-3蛋白的表达,促进Bcl-2蛋白的表达有关。
Aim：To investigate the protective effect of simdax on lipopolysaccharide（LPS）-induced neonatal rat cardiomyocyte injury.Methods： The neonatal rat cardiomyocytes were allocated into 3 groups： control group,LPS group and LPS＋simdax group.The cells in LPS＋simdax group were pretreated with simdax（0.30 μmol/L） for 24 h.The cells in LPS group and LPS＋simdax group were incubated with LPS（10 mg/L） for 6 h.The contents of LDH and CK in the culture medium were tested by automatic biochemistry analyzer,and those of TNF-α and IL-6 were evaluated by ELISA;the apoptosis was determined by flow cytometry;the expressions of Cleaved-Caspase-3 and Bcl-2 were measured by Western blot.Results： Compared with control group,the contents of LDH,CK,TNF-α and IL-6 as well as the apoptosis rate in LPS group were elevated significantly;the expression of Cleaved-Caspase-3 was increased apparently while that of Bcl-2 was reduced significantly（P〈0.05）.However,compared with LPS group,the contents of LDK,CK,TNF-α and IL-6 and the apoptosis rate in LPS＋simdax group were significantly decreased,the expression of Cleaved-Caspase-3 was reduced,and that of Bcl-2 was increased（P〈0.05）.Conclusion： Simdax may inhibit the LPS-induced neonatal rat cardiomyocyte injury via decreasing the production of proinflammatory cytokines,down-regulating the expression of Caspase-3 and up-regulating the expression of Bcl-2.
出处
《郑州大学学报（医学版）》
CAS
北大核心
2017年第4期427-430,共4页
Journal of Zhengzhou University(Medical Sciences)
基金
河南省医学科技攻关计划普通项目201602103
