STAT3、ERK、NF-κB在黄芪保护病毒感染心肌细胞中的作用

Signal transducers and activations and transcription 3,extracellular signal-regulation kinase and NF-κB are regulated by Huangqi in viral myocarditis

目的:研究STAT3、ERK、NF-κB在黄芪保护感染病毒的心肌细胞中的作用。方法:体外分离培养心肌细胞并分为对照组;病毒感染组:病毒孵育;黄芪干预组:病毒孵育后分别给予黄芪培养浓度为300 mg/L、500mg/L、700 mg/L。采用RT-PCR检测各组病毒RNA,采用W esten b lotting检测P-STAT3、P-ERK、NF-κB p65表达。MTT法观察细胞活性。结果:在各组中STAT3、ERK总蛋白没有明显变化(P>0.05),病毒组P-STAT3、P-ERK、NF-κB p65明显高于对照组(P<0.01),黄芪组P-STAT3、P-ERK、NF-κB p65明显低于病毒组(P<0.01)。黄芪组细胞存活率明显高于病毒组(P<0.01)。结论:在病毒性心肌炎中黄芪可以通过抑制STAT3、ERK、NF-κB保护心肌细胞。

AIM： To study the role of signal transducers and activations and transcription 3 （ STAT3 ）, ERK and NF-κB in early phase of viral myocarditis in the cultured cardiac myocyte reacted by Huangqi. METHODS： The cardiac myocytes of neonatal SD rat were prepared, cultured and divided into control group, virus group and Huangqi intervention groups. Virus group was inoculated with coxsackieviruses B3. Huangqi group was inoculated with Huangqi at concentration of 300 mg/L, 500 mg/L or 700 mg/L after infected with CVB3. Control group was treated with same dose of DMSO. Western blotting was used to study the protein of ERK and phosphor - ERK, STAT3 and phosphor - STAT3, NF - KB p65. Cell viability was analyzed with 3 - （4,5） dimethylthiazole - 2 - yl - 2, 5 - diphenyl - tetraoliumbromide （ MTT）. RESULTS ： The total proteins of ERK and STAT3 were not difference （P 〉 0. 05）. However, phosphor - ERK and phosphor - STAT3, NF -κB were higher in CVB3 group than those in control groups （P 〈 0. 01 ）. Phosphor - ERK, phosphor - STAT3 and NF -κB in Huangqi group were lower than those in CVB3 group （P 〈0. 01 ）. Cell viability in Huangqi group was higher than that in CVB3 group （P 〈 0. 01 ） by MTT assay. CONCLUSION： Huangqi protected myocytes in viral myocarditis by blocking the activity of STAT3, ERK and NF -κB.