目的通过建立C57BL/6小鼠动脉粥样硬化模型探讨CD4+CD25+调节性T细胞( Treg)在动脉粥样硬化发病及治疗过程中的作用。方法24只雄性C57BL/6小鼠随机分为3组：正常对照组、动脉粥样硬化组、阿托伐他汀组。正常对照组给予基础饲料,其余组给予高脂饲料。高脂饲养4周后,阿托伐他汀组继续高脂饲养并加用阿托伐他汀干预,3组共观察16周。苏木精染色观察血管病变情况,流式细胞仪检测外周血CD4+CD25+Treg的表达情况, ELISA法检测外周血TGF-β浓度。结果①动脉粥样硬化组的动脉血管的内膜显著增生,CD4+CD25+Treg/CD4+T细胞比例显著低于正常对照组,差异有统计学意义( P<0．01)。阿托伐他汀组的动脉血管较动脉粥样硬化组病变明显减轻。阿托伐他汀组的CD4+CD25+Treg/CD4+T细胞比例较动脉粥样硬化组有显著提升(P<0．01),与正常对照组差异无统计学意义。②动脉粥样硬化组TGF-β浓度较正常对照组明显降低( P<0．01)。阿托伐他汀组的 TGF-β的浓度显著高于动 脉粥样硬化组( P<0．01)；较正常对照组略低,差异无统计学意义。结论 CD4+CD25+Treg及其分泌的TGF-β具有抑制动脉粥样硬化发展的作用,有望成为治疗动脉粥样硬化的新靶点。%Objective To investigate effects and mechanism on CD4 +CD25 +Treg in C57 BL/6 mice model of ath-erosclerosis. Methods Twenty-four male C57BL/6 mice were assigned to three groups:control group, atherosclero-sis group and atorvastatin group. Control group was given normal diet, and the rest groups were given high fat diet. After 4 weeks of high fat diet,atorvastatin group was continued to keep high fat diet and given drugs. The mice were observed for 16 weeks. Vasculopathy was analyzed by hematoxylin-eosin staining. Expression of CD4 +CD25 +Treg in peripheral blood was analyzed by flow cytometry. Concentration of TGF-β was analyzed by ELISA. Results ①Hyperplasia of intima was observed in AS group, and the percentage of CD4 +CD25 +Treg/CD4 + T cell was signifi-cantly lower than that of the control group(P<0. 01). Atatorvastatin could significantly reduce the intimail thick-ness. The percentage of CD4 +CD25 +Treg/CD4 + T cell was significantly higher than that of AS group(P<0. 01). Atorvastatin group and control group had no significant difference.②As group′s concentration of TGF-βwas signif-icantly lower than the control group(P<0. 01). Atorvastatin group′s concentration of TGF-βwas significantly high-er than that of AS group(P<0. 01). Atorvastatin group and control group had no significant difference. Conclu-sion Our date provides evidence to show CD4 +CD25 +Treg and autocrine secretion of TGF-β can inhibit the de-velopment of atherosclerosis,and they will be a new therapeutic target of atherosclerosis.
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