菊苣酸对脂多糖诱导的H9C2细胞损伤的保护作用及机制

Protective effects of chicoric acid on LPS-induced H9C2 cells injury and its mechanism

目的,研究菊苣酸(chicoric acid,CA)预处理在脂多糖(1ipopolysaccharide,LPS)诱导的损伤中对心肌细胞的保护作用及机制。方法用LPS对大鼠心肌细胞H9C2进行诱导损伤,评估不同浓度CA对心肌细胞的保护作用。CCK-8法检测细胞活力,化学比色法检测细胞内活性氧(ROS)释放量,流式细胞学检测细胞的凋亡率,Western blot检测沉默信息调节因子1(SIRT1)、核转录因子-κB(NF-κB)、IκBa、Caspase-3的表达。结果LPS可降低细胞活力,显著增加细胞内ROS的生成量,同时升高NF-κB、Caspase-3的表达,降低IκBα、SIRT1的表达水平,而CA预处理可以减轻LPS对细胞的损伤,减少ROS生成,同时减少NF-κB、Caspase-3表达,升高IκBa、SIRT1表达(P<0.05)。结论CA可通过调节SIRT1/NF-κB信号通路抑制LPS诱导的H9C2细胞损伤。

Objective To study the protective effect of chicory acid (CA)on cardiomyoeyte injury induced by lipopolysaccharide (LPS)and its mechanism.Methods LPS was used to induce H9C2injury in rat cardiomyocytes,and the protective effect of different concentrations of CA on eardiomyocytes was evaluated.The cell viability was measured by CCK -8 assay.The release of LDH and ROS in LPS -injured cells was detected by flow cytometry.Western blot was used to detect the expression of SIRT1,NF-κB,IκBα,Caspase-3.Results LPS reduced cell viability,increased ROS and LDH production,increased NF -κB and Caspase -3 expression,and decreased the expression of I -κBα and SIRT1,but all these effects were partially but significantly reversed by CA pretreatment. Condusion CA can inhibit LPS -induced injury of H9C2 cells through regulating SIRT1/NF -κB signaling pathway.