粒细胞集落刺激因子对心肌梗死大鼠心肌T细胞亚群的影响

Effects of G-CSF on T Lymphocyte Subpopulations of Myocardium in Rats with Myocardial Infarction

目的:探讨粒细胞集落刺激因子(G-CSF)对心肌梗死大鼠心肌T淋巴细胞亚群的影响。方法:29只大鼠随机分为干细胞动员组(GAMI,n=9)、心肌梗死对照组(AMI,n=10)和假手术组(SO,n=10)。GAMI组和AMI组结扎左冠状动脉造成心肌梗死,SO组行相似的手术操作但不结扎冠状动脉。GAMI组给予rhG-CSF(50μg·kg-1·d-1),皮下注射,共7d。AMI组及SO组则每日皮下注射同等体积的生理盐水,共7d。心肌梗死后4周,通过免疫组化染色检测心肌CD3+、CD4+和CD8+细胞计数并计算CD4+/CD8+比率。结果:AMI组大鼠有3只分别于术后第3、7、8天死亡,GAMI组与SO组大鼠至观察结束无一只死亡。与AMI组相比较,GAMI组CD3+和CD8+细胞计数降低(均P<0.01),CD4+细胞计数无明显变化(P>0.05),CD4+/CD8+比率升高(P<0.01)。结论:G-CSF可降低心肌梗死后大鼠心肌CD3+和CD8+T淋巴细胞计数、升高CD4+/CD8+比率,提示G-CSF可减轻心肌梗死后的免疫损伤。

Objective： To investigate T lymphocyte subsets changes affected by treatment of G-CSF in acute myocardial infarction rats. Methods： Twenty-nine rats were randomly divided into there groups, GAMI（n = 9）,AMI（n = 10） and SO（n = 10）. The left coronary artery was ligated in GAMI and AMI groups result in AMI and sham-operation was performed in SO group. Rats of GAMI group were subcutaneously injected with rhG-CSF（50μg·kg^-1·d^-1） for seven days. Saline was given by the same manner in the sham-operated and the AMI group for seven days, After four weeks of infarction, the number of CD3^＋,CD4^＋ and CD8^＋ cells per field of a microscope was detected and CD4^＋/CD8^＋ ratio was obtained through the stain of immunohistochemistry. Results： Three rats in the AMI group died on the third,seventh and eighth day after myocardial infarction, No rats died in GAMI and AMI groups. A significant decrease in the number of CD3^＋ and CD8^＋ cells per field combined with a significant increase in CD4^＋/CD8^＋ ratio were documented in the GAMI group （P 〈 0.01, P 〈 0.01） respectively and there was no statistic significance in CD4^＋ cells （P 〉 0.05）compared with the AMI group. Gonclusion： The treatment of G-CSF can reduce the number of CD3^＋, and CD8^＋ per field ,enhance CD4^＋/CD8^＋ ratio in rats with myocardial infarction. These findings suggest that G-CSF may play an important role in relieving the immune injury induced by T lymphocyte in acute myocardial infarction rats.