Welcome to Chinese Journal of Clinical Pharmacology and Therapeutics,Today is Chinese

Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2018, Vol. 23 ›› Issue (5): 498-503.doi: 10.12092/j.issn.1009-2501.2018.05.003

Previous Articles     Next Articles

Effects of MG-132 on cardiomyocyte apoptosis factor of CVB3 viral myocarditis in mice

ZHANG Xinmin, CHEN Peng,YE Sheng, XIA Wujie, LI Yuechun   

  1. Department of Cardiology, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, China
  • Received:2018-01-10 Revised:2018-02-22 Online:2018-05-26 Published:2018-05-16

Abstract:

 AIM: To observe the effects of proteasome inhibitor MG-132 on myocardial cell apoptosis factor in mice with viral myocarditis, and further to explore the specific mechanisms of the ubiquitin proteasome system in the process of apoptosis in viral myocarditis.METHODS:Ninety male BALB/C mice were randomly divided into 3 groups: the normal control group (n=30), the myocarditis group (n=30), and the myocarditis +MG-132 treatment group (n=30). Intraperitoneal inoculation of coxsackievirus B3 virus (CVB3) was used to induce acute myocarditis. The treatment group was injected with proteasome inhibitor MG-132 intraperitoneally for a consecutive 7d. The control group and myocarditis group were intraperitoneally injected with DMSO solvent. The survival rate of mice, cardiac function index, pathology and the changes of cardiomyocyte apoptosis factors were observed on the 8th day. RESULTS: Compared with myocarditis group, the nuclear factor kappa B level in MG-132 treated group was significantly decreased (P<0.05), the level of Bax was significantly decreased (P<0.05), the level of Bcl-2 was significantly increased (P<0.05), and the Bcl-2/Bax ratio increased significantly (P<0.05). Compared with the myocarditis group, the MG-132 treatment group significantly reduced the cardiomyocyte apoptosis, the improvement of the hemodynamic status and the survival rate in the myocarditis mice. CONCLUSION: Proteasome inhibitor MG-132 can inhibit the apoptosis of cardiomyocytes and improve the cardiac function and survival rate in mice with acute viral myocarditis by down-regulating nuclear factor kappa B and Bax and up-regulating Bcl-2 level.

Key words: viral myocarditis, MG-132, apoptosis, NF-kappaB, Bcl-2, Bax

CLC Number: