摘要
目的 探讨黄芪在保护病毒性心肌炎 (VM)心肌细胞中信号转导及转录活化因子- 3(STAT3)表达及其对细胞增殖的影响。方法 体外分离培养心肌细胞建立VM心肌细胞模型。采用不同浓度黄芪进行干预 ,RT- PCR、Westernblot、MTT等方法分别检测各组病毒RNA及STAT3水平变化。结果 黄芪干预组细胞病毒RNA表达均减弱 ,而且与浓度无关 (P >0 .0 5)。Westenblot法示黄芪对STAT3有抑制作用 ,而且浓度越高 ,抑制作用越强 (P <0 .0 1 )。MTT法示黄芪为 1g/L时细胞出现病变 ,70 0mg/L时细胞存活率最高。结论 黄芪可以抑制病毒RNA复制 ,其保护作用与抑制STAT3信号通路密切相关。
Objective To investigate the expression of signal transducers and activations and transcription 3(STAT3)in protecting cardiacmyocyte in children with viral myocarditis and the effect of astragaluson on cellular proliferations.Methods Neonatal SD mice cardiac myocyte cultures are prepared with enzymatic digestion, and incubated. CVB_3 group was inoculated with coxsackieviruses B_3;astragalus group was inoculated after being infected with CVB_3; control group was treated with same dose DMSO. Western Blot was used to study the protein of STAT3 and P-STAT3.Cell viability was analyzed by MTT.CVB_3 mRNA was analyzed by RT-PCR.Results The protein concentration of STAT3 has not different(P>0.05). But the activation of STAT3 was higher in CVB_3 group than control groups(P<0.01). And the protein of P-STAT3 in study group was lower than CVB_3 group(P<0.01), moreover the concentration of astragalus affected the activation of STAT3. In MTT, cell viability in astragalus group was higher than CVB_3 group(P<0.01).Conclusion Astragalus could block the viral mRNA duplication and its protective role is closely related to STAT3.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2005年第3期218-220,i001,共4页
Journal of Applied Clinical Pediatrics
基金
卫生部科学研究基金资助 (98- 1 - 1 38)
关键词
信号转导及转录活化因子-3
心肌炎
病毒性
黄芪
signal transducers and activations and transcription 3
viral myocarditis
astragalus