中文摘要：

目的通过研究硒含量对大鼠心肌细胞Toll样受体2（TLR2）、细胞间黏附因子-1（ICAMl）、生长停滞与DNA损伤诱导蛋白45d（Gadd45α）基因调控作用，探讨硒对克山病的表观遗传可能的影响机制。方法通过建立不同硒含量饲喂sD大鼠动物模型、培养新生代缺硒大鼠心肌细胞与正常大鼠及其心肌细胞比较，使用RT—PCR、免疫印迹分析等方式，研究硒含量对心肌细胞TLR2、ICAMl、Gadd45α的表观遗传调控及基因表达的调节机制。结果喂食缺硒（0．1mg／kg）饲料大鼠比喂食充足硒饲料（2mg／kg）大鼠的DNA甲基化水平更低，但TLR2、mRNA和蛋白水平更高（P〈0．05）；缺硒环境的心肌细胞（TLR2和ICAMl）启动子的甲基化水平显著降低，但TLR2和ICAMlmRNA和蛋白水平更高；随着硒含量增加，Gadd45α表达、TLR2启动子甲基化水平和TLR2的表达水平逐渐降低。结论硒处理，可能是通过调控Gadd45ct因子表达，抑制DNA去甲基化和炎症因子（TLR2、ICAMl）的表达，从而保护因炎症性细胞因子过度表达引起的大鼠心肌损伤。

英文摘要：

Objective To study the effect of selenium （se） on rat myocardial cell of TLR2, ICAM1, Gadd45α gene,to explore the content of selenium on pigenetic regulatory mechanisms in patients with Keshan disease. Methods The effect on selenium content of myocardial cell of TLR2, ICAM1, Gadd45α epigenetic regulation of gene expression and regulation mechanism were investigated through the establishment of animal model of SD rats, training new generation of rat cardiomyocytes, comparing with the normal rats and myocardial cells, analysis by RT - PCR, western blot analysis, etc. Results Feeding deficiency Se SD rats have significantly low of DNA methyl of level than feeding sufficient Se feed （2 mg/kg） SD rats, but TLR2, and mRNA and protein level were significantly high （ P 〈0.05 ）. Deficiency Se environment of myocardial cell has significantly more low expression of （TLR2 and ICAM1 ） promoter of methyl level, but significantly more higher expression of TLR2 and ICAM1 mRNA and protein level. Gadd45α express, TLR2 promoter methylation and expression of TLR2 levels gradually reduced with selenium content increasing. Conclusion Selenium may modulate possibly through regulation of expression of Gadd45α factor, inhibiting DNA methylation and expression of inflammatory factors. These processes can protect injury because of the over - expression of inflammatory cytokine - induced myocardial in rats.