慢性炎症反应是心梗后心室重构的主要原因。效应性Th1和Th17细胞促进心梗后炎症反应和心室重构。本研究小组前期发现，Tregs可有效抑制Th1和Th17细胞反应。最近发现HIF-1α可调节Tregs和Th17细胞分化。因此，心梗局部低氧微环境诱导的HIF-1α可能破坏Tregs/T效应细胞平衡，促进炎症反应和心室重构。本研究拟使用流式细胞仪和免疫组化技术检测小鼠心梗模型中HIF-1α，Tregs和Th17细胞的表达,病理学和心超检查心梗后炎症反应和心室重构。基因芯片和免疫荧光评价Cx43对心肌Tregs功能的影响及这群Tregs对心梗后炎症反应的作用。ELISA和PCR检测体外共培养中Tregs对心肌细胞活性的影响及HIF-1α对Tregs功能的抑制作用， 明确HIF-1α介导的Tregs/Th17细胞失平衡促进心梗后慢性炎症反应的机制，为合理进行心梗后心室重构的干预提供实验依据。

Chronic inflammation lead to left ventricular(LV) remodeling after myocardial infarction (MI). Activation of Th1 and Th17 responses promote the inflammation and LV remodeling after MI. We previously reported that adoptively transfer of Tregs down regulate Th1 and Th17 responses and attenuate Th1 and Th17 mediated disease. Recent studies revealed the vital role of HIF-1α in promoting the differentiation of Th17 cells and inhibiting Tregs. Our hypothesis is that hypoxia in the MI region inducing high levels of HIF-1α，disturb the balance of Tregs/Th17 cells and contribute to the chronic inflammation and LV remodeling. In this project, we will detect the expression of HIF-1α，FoxP3 and IL-17 by FACS and immunohistochemistry. LV remodeling will be evaluated by echocardiography and inflammation by pathological examination. Gene microarray and immunofluorescence will be used to analyze the expression of Cx43 and the characteristics of myocardium Tregs. Viability and apoptosis will be detected by ELISA and PCR after coculture of Tregs and primary myocardial cells. This project may partly uncover the mechanism of HIF-1α mediated Tregs/Th17 imbalance in chronic inflammation after MI and provide possible strategies to prevent the progression of LV remodeling after MI.