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目的研究高血脂对小鼠Foxp3基因表达的影响,并观察ApoE-/-小鼠动脉粥样硬化中Foxp3的表达及鉴定其功能。方法选取8周龄雄性C57BL/6JApoE-/-及其同系野生型小鼠16只,分为对照组和高脂饮食组(n=8),构建小鼠动脉粥样硬化模型,比较不同组小鼠血脂水平、斑块面积和不同器官组织中Foxp3+CD4+CD25+Tregs细胞的数目;利用RT-PCR和Western blot分析组织中Foxp3基因转录水平和Foxp3蛋白表达水平。结果与对照组[TG(2.0±0.1)mmol/L、TC(20.6±0.1)mmol/L]比较,高脂饮食组小鼠血脂水平[TG(2.8±0.2)mmol/L、TC(28.2±1.2)mmol/L]明显升高(P<0.01),斑块面积(25044.32±4920.42)μm2显著增加(P<0.01),而不同器官组织中Foxp3+CD4+CD25+Tregs细胞的数目显著减少(P<0.05),Foxp3基因转录水平(P<0.01)和Foxp3蛋白表达(P<0.05)降低。结论高脂能抑制不同免疫器官Foxp3基因的表达和功能,可能是高脂致动脉粥样硬化的机制之一。
Objective To investigate the effect of hyperlipidemia on Foxp3 gene expression in mice and to observe the expression of Foxp3 in ApoE - / - mice and its function. Methods Sixteen 8-week-old male C57BL / 6JApoE - / - and their homologues wild type mice were divided into control group and high-fat diet group (n = 8) to construct the model of atherosclerosis in mice. Rat blood lipids, plaque area and the number of Foxp3 + CD4 + CD25 + Tregs cells in different organs. The transcription level of Foxp3 and the expression of Foxp3 in tissues were analyzed by RT-PCR and Western blot. Results Compared with the control group [TG (2.0 ± 0.1) mmol / L, TC (20.6 ± 0.1) mmol / L] (P <0.01). The plaque area (25044.32 ± 4920.42) μm2 increased significantly (P <0.01), while the number of Foxp3 + CD4 + CD25 + Tregs cells in different organs decreased significantly P <0.05). Foxp3 gene transcription (P <0.01) and Foxp3 protein expression (P <0.05) decreased. Conclusion High-fat can inhibit Foxp3 gene expression and function in different immune organs, which may be one of the mechanisms of atherosclerosis caused by hyperlipidemia.