Effects of matrine on akt protein expression in mice with viral myocarditis
10.3760/cma.j.issn.1003-9279.2010.04.013
- VernacularTitle:苦参碱对病毒性心肌炎小鼠蛋白激酶B表达的影响
- Author:
Yong-Mei SUN
1
;
Gui-Lan CHU
;
Yan-Yan HAN
;
Jing-Hui SUN
Author Information
1. 天津医科大学总医院
- Keywords:
Myocarditis;
Coxsackievirus infections;
Apoptosis;
Protein kinases;
Matrine
- From:
Chinese Journal of Experimental and Clinical Virology
2010;24(4):276-278
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of Matrine on Akt protein expression in the myocardial tissue in mice with viral myocarditis(VMC) and to approach Matrine's protective mechanism.Methods Four-week-old healthy male Balb/c mice were inoculated intraperitoneally with 0.2ml of 100TCID50 Coxsackie virus B3(CVB3) every day(the.total is for 3 days) to construct VMC animal model. A total of 120 mice were randomly divided into 6 groups:Matrine treatment groups including high does(80 mg/kg), midst does (40 mg/kg) , lower does (20 mg/kg); Ribavirin group; virus group and control group.The medicine treatment groups were injected intraperitoneally with equal volume solution starting from 60minutes after CVB3 were inoculated in the last time, the total days of administering medicine is for10 days.And control group were injected with 0.2ml of 0.9% sodium chloride instead of medicine. Six animals were killed in the 5th and the 10th day after administering medicine in each group for determination apoptosis (by Tunel method). Protein expression of Phospho-AktSer-473 were detected in the 10th day after treatment (by immunohistochemistry and Western Blot respectively). Results Compared with control group, apoptotic cells in virus group were increased (P＜0.05). The groups of Matrine treatment can significantly decrease apoptosis of myocardial tissue of VMC animals, and Matrine(40 mg/kg) can significantly increase phosphorylation of Aktser-473 in the myocardial tissue as compared with virus group. Conclusion Matrine can reduce myocardium apoptosis of VMC animals by promoting phosphorylation of AktSer-473 in the myocardial tissue to provides concrete protection against CVB3 infection.
