槲皮素通过抑制Caspase3/Bax/Bcl-2凋亡通路保护内毒素血症小鼠心肌损伤

Quercetin Protects Myocardial Injury in Endotoxemia Mice by Inhibiting Caspase3/Bax/Bcl-2 Apoptosis Pathway

目的:观察槲皮素对内毒素血症小鼠心肌损伤的保护作用,并探讨Caspase3/Bax/Bcl-2凋亡信号通路机制。方法:18只C57BL/6N小鼠随机分为对照组(Control组)、脂多糖诱导内毒素血症模型组(LPS组)、槲皮素治疗组(QR组)。酶联免疫吸附测定法(ELISA)检测小鼠血清中cTnI、LDH、CK-MB、TNF-α、IL-1β和IL-6水平;心脏超声检测小鼠LVEDd、LVESd、EF、FS、CO等心脏结构及心功能指标;Western Blot法检测心脏组织中Caspase3、Bax、Bcl-2的表达。结果:与Control组比较,LPS组cTnI、LDH、CK-MB、TNF-α、IL-1β和IL-6表达均升高,EF、FS、CO等心功能指标均下降,Caspase3和Bax表达增强,Bcl-2表达减弱;与LPS组比较,QR组cTnI、LDH、CK-MB、TNF-α、IL-1β和IL-6表达均下降,EF、FS、CO等心功能指标均升高,Caspase3和Bax表达减弱,Bcl-2表达增强。结论:槲皮素对LPS诱导内毒素血症小鼠心肌损伤具有保护作用,其作用机制与降低炎性因子TNF-α、IL-1β和IL-6释放,抑制Caspase3/Bax/Bcl-2凋亡信号通路有关。

Objective To observe the protective effect of quercetin on myocardial injury in endotoxemia mice,and to explore the mechanism of Caspase3/Bax/Bcl-2 apoptosis signaling pathway.Methods Eighteen C57BL/6N mice were randomly divided into control group,lipopolysaccharide-induced endotoxemia model group(LPS group),and quercetin-treated group(QR group).Enzyme-linked immunosorbent assay(ELISA)was used to detect the levels of cTnI,LDH,CK-MB,TNF-α,IL-1βand IL-6 in mouse serum.Cardiac ultrasound was used to detect mouse heart structure and heart function indexes,including LVEDd,LVESd,EF,FS,CO,etc.Western Blot method was used to detect the expression of Caspase3,Bax and Bcl-2 in heart tissue.Results Compared with the control group,the serum levels of cTnI,LDH,CK-MB,INF-α,IL-1βand IL-6 of LPS group increased,while cardiac function indicators such as EF,FS,CO decreased.the expressions of Caspase3 and Bax were enhanced,and the expression of Bcl-2 expression was weakened.Compared with LPS group,the expression of cTnI,LDH,CK-MB,TNF-α,IL-1βand IL-6 in the QR group were all decreased,EF,FS,CO and other cardiac function indexes were all increased.The expressions of Caspase3 and Bax were weakened,and the expression of Bcl-2 was enhanced.Conclusion Quercetin has a protective effect on myocardial injury in LPS-induced endotoxemia mice,and its mechanism is related to reducing the release of inflammatory factors TNF-α,IL-1βand IL-6,and inhibiting aspase3/Bax/Bcl-2 apoptosis signaling pathway.