SHENQI FUZHENG INJECTION IMPROVES CVB3-INDUCED MYOCARDITIS VIA INHIBITING TRAF6 EXPRESSION
SHENQI FUZHENG INJECTION IMPROVES CVB3-INDUCED MYOCARDITIS VIA INHIBITING TRAF6 EXPRESSION
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DOI：
10.1170/216
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发表时间：
2013-01-01
影响因子：
1.6
通讯作者：
Wu, T.
中科院分区：
文献类型：
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作者：
Chen, J.;Wang, Z.;Wu, T.
病毒性心肌炎是由柯萨奇B3病毒(CVB3)感染引起的以心脏炎症为特征的青壮年心力衰竭的主要原因。然而，针对炎症和炎症反应途径的有效治疗仍然缺乏。参七扶正注射液在心血管疾病中有着广泛的应用。但参附子对急性病毒性心肌炎时的心脏炎症是否有影响尚不清楚。本研究旨在探讨参附子对柯萨奇病毒B3所致心肌炎的保护作用。120只小鼠经腹腔接种CVB3建立急性病毒性心肌炎模型。以CVB3感染小鼠为模型，观察小鼠体重、死亡率。采用逆转录聚合酶链式反应、免疫印迹和免疫组织化学方法检测心肌组织中TRAF6的表达。我们发现，在CVB3诱导的心肌炎的发展过程中，TRAF6mRNA和蛋白的表达显著且持续增加。CVB3诱导的心肌组织中CK、CK-MB、LDH、AST等血清酶活性也明显升高。值得注意的是，注射参附子显著减少了CVB3诱导的TRAF6的产生，并减轻了心肌炎的严重程度。本研究证实了参附子对CVB3所致心肌炎的保护作用，为病毒性心肌炎的治疗探索了新的治疗策略。
Viral myocarditis is a main cause of heart failure in young adults, which characterized by cardiac inflammation and caused by Coxsackievirus B3 (CVB3) infection. However, efficient therapies targeting inflammation and inflammatory response pathway are still elusive. Shenqi Fuzheng injection (SQFZI) is extensively applied in the cardiovascular diseases. But whether SQFZI may affect cardiac inflammation during acute viral myocarditis remains to be elucidated. The purpose of the present study was to investigate the potential protective effect of SQFZI on CVB3-induced myocarditis. Total of 120 mice were intraperitoneally inoculated with CVB3 to establish acute viral myocarditis model. For the CVB3-infected mice model, the body weight, mortality was observed. RT-PCR, western blot and immunohistochemistry methods were selected to detect the TRAF6 expression in myocardial tissues. We found that the expression of TRAF6 mRNA and protein were markedly and persistently increased during the progression of CVB3-induced myocarditis. The serum enzymes activity, including CK, CK-MB, LDH, AST, were also enhanced in CVB3-induced myocardial tissues. Notably, injection with SQFZI remarkably reduced CVB3-induced TRAF6 production and alleviated the severity of myocarditis. This study demonstrates the protective role of SQFZI against CVB3-induced myocarditis, which may explore a new therapeutic strategy for the treatment of viral myocarditis.