Objective:To investigate the role of STAT3 in the pathogenesis of acute viral myocarditis(VCM)in mice and its possible mechanism.Methods:Acute VCM mice models were established forty-five mice were randomly divided into blind control group (n=10)

virus-infection control group(n=15)

RPMintervention group(n=20).In RPM intervention group

RPM was given to mice intraperitoneally once a day with general dosage of 0.4 mg(/kg·d)at 24 hours before infected with coxsackie virus B3

mice of virus-infection control group were given the same volume of Dulbcco’s Modifed Eagle Medium and virus.Blind control group was only given the same volume of Dulbcco’s Modifed Eagle Medium

but not infected coxsackie virus B3.Twelve days later

the general condition and survival rate of mice were observed and then all experimental mice were sacrificed patholog and detecting CVB3 virus titer in myocardium. And double-sandwich ELISA was used to detect the levels of IFN-γ

and TNF-αin the serum.Results:The pathological changes of myocardium of the mice in RPM intervention displayed more seriously than the mice with acute VMC and both the cytokines expressions in the serum of RPM intervention group were higher than those of the acute VMC group

but there was no significant difference in the virus titer between the two groups.Conclusions:The activation of STAT3 can somehow protect myocardial tissues during the incidence of viral myocarditis in mice to inhibit its activation and improve the sensibility of mice to CVB3

although the activation of STAT3 cannot affect CVB3 virus replication

it can inhibit the over-expression of IFN-γand TNF-αto weaken myocardial damage.