白介素-38通过抑制白介素-17的表达从而保护心肌梗死后心室重构的作用及机制研究

Ventricular remodeling after acute myocardial infarction（AMI) is a chronic inflammatory process, our study have dicovered that Interleukin(IL)-17 promote ventricular remodeling after AMI, but its upstream factor which could inhibit its role of proinflammation have not be clear. IL-38 is a member of IL-1 family，involved in autoimmune diseases，but its biological activity is unclear.On the base of my reserch that IL-38 mRNA expression level in myocardium after AMI is higher than control group in mice and supplementing IL-38 can optimize the function of heart ,we will reveal the role and mechanism of IL-38 on cardiomyocyte apoptosis, and try to clarify the relation between IL-38 and IL-17.This subject is to prove that IL-38 is involved in ventricular remodeling after AMI,completing the system of the inflammation in ventricular remodeling after AMI,maybe contribute to the future therapy of heart failure.

急性心肌梗死(acute myocardial infarction, AMI)后心室重构是一个慢性炎症性疾病，申报者前期研究证明白介素(interleukin , IL)-17的促炎作用恶化了AMI后心室重构，但抑制IL-17的上游因子尚无定论。IL-38是IL-1家族的一员，介入于自身免疫性疾病，我们前期发现IL-38在梗死后小鼠心肌中表达增高，且在体补充IL-38细胞因子可优化心功能。在此基础上，我们拟在小鼠心肌梗死模型上，观察IL-38的表达规律，对心功能、心肌细胞凋亡的影响并探讨其与IL-17的相互作用，以论证IL-38在心肌梗死后心室重构中的作用及机制，证明IL-38是保护心肌梗死后心室重构的一个新的细胞因子。本课题的研究有望阐明IL-38在梗死后心室重构中的作用机制，完善梗死后心室重构的免疫炎症理论，为心肌梗死后心衰的靶向治疗提供新的实验依据。