The Effect Of Myocardium Oxyradical In Viral Myocarditis Mice On P38MAPK And The Intervention Effect Of Edaravone

viral myocarditis(VMC)is a very frequent acquired heart disease for children, from1956 Janett first report, the morbidity riseyear by year. VMC is a subtype of infectious cardiomyopathies, which means viral infection injury the myocardium or autoimmune response produce coup injury, also can produce endocardium,pericardium and other organ inflammatory changes, due to some extent heart failure and body symptom. The virus that cause myocarditis is various,especially CVB, which is a single strand RNA virus, micro-RNA virus, Enterovirus genus, the pathogenesy is unclear, usually deem in the initial stage of virus infection,virus invasion myocardium produce acute inflammatory reaction, myocardiolysis, degeneration, or cell infiltration, that severe chronic myocardium pathological changes is immunity mediated. Recently investigation indicated oxygen free radical caused myocardial damage, which make effect on unsaturated fatty acid in biomembrane, initiated lipid peroxidation, produced cadiocyte ischemia, membrane permeability increasing, calcium ion inflow, intracellular calcium overload, myocardiolysis,fibroplasia and scarring, meantime erythrocytic SOD activity depress, as the free radical, nucleate segmentation,polysaccharides depolymerize,unsaturated fatty acid peroxidation, cytomembrane damaged, caused myocarditis. For the past few years research indicated, apoptosis maybe one of the important pathogenesy in viral myocarditis, oxygen free radical activated p38MAPK, then induceapoptosis.Edaravone as radical scavenger can inhibit xanthine oxidase and hypoxanthine oxidase, stimulate prostacyclin production, decrease mediators of inflammation leucotriene, decrease hydroxy radical concentration. Through offer electron to remove hydroxy radical inhibit free radical and cell membrane lipid peroxidation cascade reaction, active suppression Oxygen Free Radical(OFR)Mediated protein,nucleinic acid nonreversible katogene, then protect cell.This research adopted CVB3 as pathogen infected mouse, construct VMC model successfully. 75 mouses infected CVB3,69 morbility, the morbility is 92%. Detect myocardial p38MAPK, myocardial virus load, myocardial pathology integration, serum SOD,MDA, approach OFR to p38MAPK and edaravone intervention effect. This research application CVB3 infected ICR mouse to establish VMC model, recipe myocardial tissues, detect cadiocyte p38MAPK after CVB3 infection 4,7,10,14,21 days, simultaneous determination serum SOD,MDA and myocardial virus load, myocardial pathology integration, observe CVB3 infective dose,infective time to myocardial pathology integration effect, the relationship between serum SOD,MDA and myocardial tissues p38MAPK, the intervention effect of large,middle,small dosages, offer new rationale and experimental foundation to VMC pathogenesy and treatment.Results: 1. Measure CVB3 TCID50=10-6.49; 2. Construct VMC model successfully; 3. VMC mice myocardial pathology changes are myocardial necrosis and ponderosus inflammatory cell infiltrate, after edaravone treat above-mentioned changes improved; 4.The virus titer is maxlmum in the 4th day after VMC mouse conceive virus, gradually downtrend, detect no virus titer in the 21th day; 5.In mouse myocardial tissues virus group p38MAPK expression is the most, p38MAPK of treat group reduce as edaravone increase; 6.In mouse serum SOD of virus group decreased obviously, treat group increased as edaravone increase; In mouse serum MDA of virus group increased obviously, treat group decreased as edaravone increase.Conclusions: 1,CVB3 VMC mouse model affects p38MAPK expression; 2,Edaravone can clean up OFR of CVB3 VMC mouse model; 3,Edaravone can inhibit p38MAPK activation of CVB3 VMC mouse model myocardial tissues.