Part1. Rosiglitazone Attenuates Myocardial Injury Through Inhibiting The Expression Of IL-17 In Mice With Autoimmune Myocarditis Part2. Exploration On Relevance Between IL-35 And Stability Of Atherosclerotic Plaque In Patients With Coronary Atheroscleroti

ObjectiveThis study intends to explore the therapeutical effect and the pathagenesis of rosiglitazone,agonist of peroxisome proliferator activated receptor gamma,on mice with experimental autoimmune myocarditis by detecting the peripheral blood and myocardium.We are looking forward to providing a new point to study the pathgenesis and supplying a extraordinary idea to therapy.Methods70 BALB/c mice were randomly divided into 4 groups:rosiglitazone group(group A), rosiglitazone+GW9662 group(group B), myocarditis group (group C) and normal group(group D).The cardiac myosin of porcine was injected subcutaneously in group A,B and C to establish the model of EAM. The cardiac myosin (200ug per mouse,about 20ul per mouse)and the same volume of complete Freund’s adjuvant were injected into the armpit and the groin of per mouse in group A、B and C subcutaneously.Mice in group D were injected with the same volume of PBS and complete Freund’s adjuvant as group A、B and C. Mice in group A were given a intraperitoneal injection with rosiglitazone(10mg/kg) and group B was injected with rosiglitazone and GW9662.Mice in group C and D were injected with PBS.All the mice were killed at the 25th day for ELISA. Hematoxylin-Eosin immunohistochemistry and real-time PCR.ResultsIn group A, the results of ELISA and real-time PCR were lower than group B and C.However,no differences were found between group C and D. The results of Hematoxylin-Eosin showed,more inflammatory cells were found in myocardium in group B and C than in group A. As the results of immunohistochemistry showed,there were more brown cells infiltrated in myocardium in group B and C than in group A.ConclusionPpar γ signal passage was involved in the inflammatory reaction of myocardium in mice. Activating ppar γ signal passage with rosiglitazone could alleviate the inflammatory reaction in myocardium through inhibiting the expression of IL-17.Objective:In this study,we examined the stenosis and structure as well as the stability of the plaque in the criminal coronary of the patients who were hospitalized with CAD through CAG and IVUS.Fasting peripheral blood was gained after patients were admitted to the hospital.Detection of IL-35 was executed with ELISA and prediction of IL-35 to stability of plaque was made through analyzing the correlation between IL-35 in peripheral blood and remodeling index gained through IVUS.We were looking forward to supplying an effective predictor to recognize the unstable plaque.Method:45 patients who were diagnosed as coronary heat disease and were going to be treated with CAG and IVUS were involved in this study. Peripheral blood of the patients were gained before any drugs were used. Patients who had a renal failure,infection,cancer,antoimmune disease and accepted the treatment of immunosuppressive agents currently were excluded. IL-35 was detected through ELISA with the serum gained after centrifugation.Correlation between serum IL-35 detected through ELISA and coronary remodeling index obtained by IVUS.The study was permitted by Institutional Ethics Committee of shandong provincial hospital and all the patients were informed the concrete process.Results:Through detection of IVUS,the coronary intima of all the patients has a different degree of incrassation.The image of IVUS shows us that the remodeling index of patients whose coronary has a positive remodel is higher than these whose coronary has no change or has a negtive remodel.The remodeling index of coronary has a negtive correlation with IL-35 in peripheral blood.The related coefficient is -0.633.Conclusion:For patients who had CAD,the lower the IL-35 is,the higher the remodeling index is.These patients would have a less stable plaque and more likely to have acute coronary disease.IL-35 in peripheral blood is a good predictor to the stability of the atherosclerotic plaque.