热应激诱导的心肌细胞凋亡是导致心脏结构和功能损伤的原因之一。本课题组前期动物试验结果表明，微量元素锰可抑制热应激引起的肉鸡心肌细胞凋亡。然而，关于锰调控热应激诱导心肌细胞凋亡的具体分子机制尚不清楚。因此，本项目在前期研究基础上，以肉鸡心肌细胞为实验材料，体外构建热应激细胞凋亡模型，拟研究不同锰水平和锰源对心肌细胞凋亡及凋亡相关基因表达的影响，并结合蛋白质组学、生物信息学从锰对细胞凋亡中差异蛋白表达的影响，到调控网络的形成进行探讨，从而系统、深入揭示锰对心肌细胞凋亡的作用及其分子调控机制，同时从饲料营养途径有效缓解热应激心肌细胞凋亡提供新思路和科学依据。

Cardiomyocyte apoptosis is one of the causes of cardiac structural and functional damage induced by heat stress. The results of previous animal experiments indicated that microelement manganese（Mn）can inhibit apoptosis of myocardial cells induced by heat stress in broilers. However, the specific molecular mechanism of manganese-mediated heat stress-induced cardiomyocyte apoptosis remains unclear. Therefore, based on the previous research, the project we establish the model of broiler myocardial cell apoptosis heat stress-induced in vitro to study the effect of Mn levels and sources on myocardial apoptosis and the expression of apoptosis-associated genes, and revealed the key proteins, and uncovered the regulation networks used proteomics and bioinformatics. The outcomes from this project will elucidate the effect of Mn on heat stress-induced myocardial cell apoptosis and molecular mechanism, and provide a novel nutritional strategy and scientific foundation for alleviating cardiomyocyte apoptosis of heat stress on broilers.