1.Effects of Ivabradine on the expression of inflammatory cytokines in a murine model of coxsackievir-us B3-induced viral myocarditis
Nadan ZHOU ; Teng ZHANG ; Yuechun LI ; Lisha GE
Chinese Journal of Microbiology and Immunology 2013;(10):734-739
in mice with coxsackievirus B3 (CVB3)-induced viral myocarditis through a comparative study with Carve-dilol.Methods 150 BALB/c male mice were divided into four groups including control group (n=30), myocarditis group (n=40), Ivabradine treatment group (n=40) and Carvedilol treatment group (n=40). Viral myocarditis was induced by intraperitoneal injection of CVB 3 in experimental mice , while mice in the control group were injected with PBS accordingly .The mice in four groups were respectively administered with PBS, PBS, Ivabradine and Carvedilol after 24 h of infection for 14 consecutive days .Heart specimens were collected from 8 mice of each group on days 4, 7 and 14 after measuring their heart rates .The patho-logical changes in heart tissues were observed through hematoxylin e-osin staining .Semi-quantitative RT-PCR and ELISA were performed to detect the expressions of MCP -1, IL-6 and TNF-αat mRNA and protein lev-els.CVB3 RNA was quantified by semi-quantitative RT -PCR as well .Results Compared with myocarditis group, the histopathological damages in myocardium were significantly alleviated in both Ivabradine group and Carvedilol group on days 7 and 14.The expressions of MCP-1,IL-6 and TNF -αat mRNA level were up-regulated in mice treated with Ivabradine and Carvedilol as compared with those in control group .Compared with myocarditis group , the expressions of TNF-αon day4 and IL-6 on day 7 at mRNA level were reduced in Ivabradine and Carvedilol treatment groups .MCP-1 expression at mRNA level was only down-regulated in Iv-abradine group on day 7.Concluison Ivabradine treatment could alleviate histopathological damages in my -ocardium of mice with CVB3-induced viral myocarditis , which was similar to the effects of carvedilol treat-ment.The treatment effects might be associated with the down-regulation of expressions of IL-6, TNF-αand MCP-1 at mRNA and protein levels .