| Background:Viral myocarditis(VMC) has become one of the commondiseases in children.Many virus can cause this disease, they can not only causethe degeneration and necrosis of myocardial cells, but also generateendocarditis, pericarditis and inflammatory lesion of other organs. Thedisease’s clinical symptos are different. Some children have serve illness status,but others don’t have obvious symptoms. Few childrens’ disease progression isquite rapid, cause explosive myocarditis, heart failure, cardiac shock and so on.If the virus persistant infection, it can develops to a serious life-threateningdisease called Dilated Cardiomyopathy. However the pathogenesis of VMC isnot clarified thoroughly, the therapy needs further improvement. Because VMChave a serious impact on childrens’ physical health, how to illuminate thepathogenesis and the treatment of VMC has a certain theoretical and practicalsignificance.Objective:To establish the modals of VMC through BALB/c miceinfected with coxsackievirus B3,teste the ST2protein expression of myocardialcells. To make sure the mechanism of ST2protein in VMC. In this expriment,we make andrographis injection as treatment intervention. Then the therapeuticeffect of andrographis injection for VMC and the effect for ST2proteinexpression should be discussed.Methods:110male BALB/c mice, weighting16-20g, were randomlydivided into three groups:control group(n=30), VMC group(n=40), treatmentgroup(n=40). Using CVB3virus to set models.Giving andrographis injectionthrough intraperitoneal injection as intervening treatment30d. We recordeddaily status and situation of death in mice.After virus inoculation, we weighed the mice on the4thã€7thã€14thã€30th day,killed6mice randomly everytime,determined the value of CK-MB in blood serum,examined the score formyocardial necrosis and cellular infiltration, observed myocardial collagenfiber distribution in mice, tested ST2protein by immunohistochemical method.Finally we use relevant software to analyse the results.Results:(1)The mortality increased significantly in VMC groups,12mice died in30days,They had bad conditions and light weights.5mice died intreatment group, and their conditions were better. It showed that andrographiscan improve mice survival rate.(2)The CK-MB increased on the4th day afterinfection, then the value was increased continuously, and the value of CK-MBwas climbed a peak on the7th day. The value was closed to normal at the30thday. Treatment group CK-MB value was slight increased, the peak was underthe VMC group, and recovered fast.(3)The score for myocardial necrosis andcellular infiltration also increased fast in VMC group on the4th day, it reachedthe most serious period on the7th day, closed to normal at the30th day.Treatment group mice sores were not that high as VMC group. The scores werelower on every stage.(4)We found that CVF increased significantly after14thdays in VMC group, on the30th day CVF got the highest level. Treatmentgroup mice myocardial fibrosis degree was milder than VMC group. Itsuggested that andrographis injection could lower myocardial collagen fibercontent and inflammation. It has the function of myocardial protection.(5)TheImmunohistochemistry result:The contents of ST2protein in VMC group werehigher than that of control group, and this trend was enhanced with the diseasedevelopment. ST2protein expression were significantly enhanced around themyocarditis syndrome and necrotizing lesions. It suggested that inflammatorystimulation may be related to ST2protein abnormal expression. But theexpression were lower in treatment group. Liner correlation analysis showedthe contents of ST2protein with the CVF and myocardial inflammation degree was positive correlation remarkably. Andrographis injection could reduceinflammation and fibrosis degree to intervent the expression of ST2protein.Conclusion:1ã€ST2protein participate in the whole process of VMC.2ã€ST2L is involved in inflammatory response at the early satge of VMC, it playsa protective role in the development of myocardial fibrosis. sST2and ST2Lcompete with each other.3ã€Andrographis can enhance the survival rates ofVMC mice, reduce myocardial inflammation and fibrosis.4ã€Andrographis canpostpone the progress of fibrosis. |