灯盏花素通过上调miR-140表达对心肌缺血再灌注损伤发挥保护作用

摘要

建立小鼠心肌缺血-再灌注损伤模型,观察灯盏花素对心肌梗死面积,凋亡因子caspase3及miR-140表达变化影响.体外建立细胞缺血-再灌注损伤细胞模型,MTT测定小鼠心肌细胞细胞活性,通过抑制与过表达miR-140,观察灯盏花素对caspase3及其上游分子TLR4、NF-κB表达的影响.研究发现灯盏花素在体内能减小心肌梗死面积,降低caspase3 mRNA表达,增加miR-140表达.在体外,抑制miR-140表达能抵消灯盏花素的抗凋亡作用,使caspase3 mRNA及TLR4、NF-κB蛋白表达增加;过表达miR-140使caspase3 mRNA及TLR4,NF-κB蛋白表达减少.因此,我们认为灯盏花素可能是通过上调miR-140表达抑制缺血-再灌注损伤引起的心肌细胞凋亡.%In mice MIR model,the myocardial infarct size,leaves of caspase3 mRNA and miR-140 were measured after scutellarin treatment.In cardiomyocytes MIR model,cell viability were assayed by MTT,the effects of scutellarin on caspase3 mRNA and protein expression of TLR4 and NF-κB were observed when miR-140 was inhibited or overexpression.The results showed that scutellarin can decrease the area of myocardial infarction,decrease the expression of caspase3 mRNA and increase the expression of miR-140 in vivo.In vitro,inhibition of miR-140 expression can counteract the anti-apoptotic effect of scutellarin,and increase the expressions of caspase3 mRNA,TLR4 and NF-κB.Overexpression of miR-140 reduced the expressions of caspase3 mRNA and TLR4 and NF-κB,which had a similar role to scutellarin.In conclusion,scutellarincan inhibit the apoptosis of myocardial cells induced by ischemia-reperfusion injury by upregulating miR-140 expression.