Effect of IFN-lambda2 on apoptotic protein in the myocardium in mice with viral myocarditis.
- Author:
Yu-Jun NIE
1
;
Xing-Yuan HUANG
;
Shi-Hong WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Coxsackievirus Infections; drug therapy; metabolism; Cytokines; therapeutic use; Enterovirus B, Human; Male; Mice; Mice, Inbred BALB C; Myocarditis; drug therapy; metabolism; Myocardium; chemistry; Proto-Oncogene Proteins c-bcl-2; analysis; bcl-2-Associated X Protein; analysis
- From: Chinese Journal of Contemporary Pediatrics 2009;11(4):296-300
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEINF-lambda has anti-viral and anti-tumor activities. Its application in viral myocarditis (VMC) has not been reported. This study investigated the role of INF-lambda in acute VMC in mice.
METHODSForty mice were randomly divided into three groups: VMC (n=15), IFN-lambda2-treated VMC (n=15) and control (n=10). VMC was induced by an intraperitoneal injection of Coxsackievirus B3 (CVB3).The control group was intraperitoneally injected with 2% PBS. The IFN-lambda2-treated VMC group was administered with 400 ng IFN-lambda2 (0.1 mL) by subcutaneous injections daily, for 5 days. The control and the VMC groups were given equal amount of nomal saline.The surviving mice were sacrificed 9 days after IFN-lambda2 treatment. The pathological changes of heart tissues were examined under a light microscope. Bcl-2 and Bax expression in heart tissues was determined by immunohistochemistry.
RESULTSThe control group presented normal heart tissues. The INF-lambda2-treated VMC group showed significantly a lower pathological score (1.5+/-0.5) than the untreated VMC group (2.8+/-0.8) (P<0.01). Bcl-2 expression decreased (P<0.01), in contrast, Bax expression increased (P<0.01) in the untreated VMC group compared with that in the control group. INF-lambda2 treatment resulted in an increased Bcl-2 expression (P<0.01) and a decreased Bax expression (P<0.01) compared to the untreated VMC group.
CONCLUSIONSINF-lambda2 may alleviate myocardial injuries and inhibit cardiomyocytic apoptosis, thus providing protective effects on myocardial cells in mice with acute VMC.