木犀草素对小鼠急性心肌梗死后心肌细胞缺血损伤的保护作用

Role of luteolin in protecting mice against cardiomyoccyte ischemic injury after acute myocardial infarction

目的探讨木犀草素对小鼠急性心肌梗死后心肌细胞缺血损伤的保护作用。方法选择C57BL/6J成年雄性小鼠54只,随机分为假手术组(6只)、模型组(16只)、联合低剂量组(木犀草素5mg/kg,16只)、联合高剂量组(木犀草素20mg/kg,16只)。RT-PCR检测心肌细胞TNF-α、白细胞介素1β(IL-1β)和白细胞介素6(IL-6)mRNA表达,TUNEL染色检测心肌细胞凋亡,免疫印迹检测信号通路c-Jun氨基末端激酶(JNK)。结果与假手术组比较,模型组生存率明显降低(P<0.05)。与模型组比较,联合高剂量组生存率明显升高(P<0.05)。与模型组比较,联合低剂量组和联合高剂量组TNF-α、IL-1β、IL-6mRNA和磷酸化P65蛋白相对表达明显降低(P<0.05)。与联合低剂量组比较,联合高剂量组TNF-α、IL-1β、IL-6mRNA和磷酸化P65蛋白相对表达明显降低(P<0.05)。与模型组比较,联合低剂量组和联合高剂量组细胞凋亡明显下调(19.17±3.06、14.67±2.34 vs 23.33±4.80,P<0.05)。与联合低剂量组比较,联合高剂量组细胞凋亡明显下调(P<0.05)。与模型组比较,联合低剂量组和联合高剂量组磷酸化P38和磷酸化JNK明显降低(P<0.05)。与联合低剂量组比较,联合高剂量组磷酸化P38和磷酸化JNK明显降低(P<0.05)。结论木犀草素通过丝裂原活化蛋白激酶/NF-κB通路保护心肌细胞缺血损伤。

Objective To stuyd the role of luteolin in protecting mice against cardiomyocyte ischemic injury after AMI.Methods Fifty-four adult male C57BL/6J mice were randomly divided into sham operation group(n=6),model group(n=16),low-dose group(luteolin 5 mg/kg,n=16),high-dose group(luteolin 20 mg/kg,n=16).Expressions of TNF-α,IL-1βand IL-6 mRNA in cardiomyocytes were detected by RT-PCR,apoptosis of cardiomyocyte was assayed with TUNEL staining.Alteration of c-Jun was detected by Western blot.Results The survival rate was significantly lower in model group than in sham operation group and was significantly higher in highdose group than in model group(P<0.05).The expression levels of TNF-α,IL-1βand IL-6 mRNA and phosphorylated P65 protein were significantly lower in low-dose group and high-dose group than in model group and in high-dose group than in low-dose group(P<0.05).The apoptosis rate of cardiomyocytes was significantly lower in low-dose group and high-dose group than in model group(19.17±3.06,14.67±2.34 vs 23.33±4.80,P<0.05).The expression levels of phosphorylated P38 and JNK were significantly lower in low-dose group and high-dose group than in model group and in high-dose group than in low-dose group(P<0.05).Conclusion Luteolin can protect mice against cardiamyocyte ischemic injury through the MAPK/NF-κB pathway.