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目的探讨FOXP3基因甲基化在2型糖尿病肾病发病过程中的作用。方法将90名研究对象分为正常对照组、单纯糖尿病组、糖尿病肾病组。采用亚硫酸氢盐测序法检测FOXP3基因启动子区(~+2071,~+2182)的甲基化水平,以流式细胞术检测CD4~+CD25~+FOXP3~+T细胞表达率。结果单纯糖尿病组和糖尿病肾病组FOXP3基因启动子区5个Cp G位点均呈现高甲基化(100%),而正常对照组第5个Cp G位点(~+2156)可见低甲基化(90%)。与正常对照组相比,其余两组CD4~+CD25~+T细胞表达率均下降,差异有统计学意义(P<0.05)。不同组别之间CD4~+CD25~+FOXP3~+T细胞表达率差异有统计学意义(P<0.01),糖尿病肾病组低于其余两组(P<0.05)。三组之间CD4~+CD25~+FOXP3~+T细胞表达呈现随病情加重而下降的趋势。年龄、糖化血红蛋白、空腹血糖、白细胞、糖尿病病程与CD4~+CD25~+FOXP3~+T细胞表达率之间呈现负相关(P<0.05)。结论 FOXP3基因启动子区高甲基化和CD4~+CD25~+FOXP3~+T细胞表达率下调可能与2型糖尿病肾病发病相关。
Objective To investigate the role of FOXP3 methylation in the pathogenesis of type 2 diabetic nephropathy. Methods 90 subjects were divided into normal control group, simple diabetic group and diabetic nephropathy group. The methylation level of FOXP3 gene promoter region (~ + 2071, ~ + 2182) was detected by bisulfite sequencing, and the expression of CD4 ~ + CD25 ~ + FOXP3 ~ + T cells was detected by flow cytometry. Results The five CpG sites in the FOXP3 gene promoter region were hypermethylated (100%) in the diabetic and diabetic nephropathy groups, while the hypomethylated (+ 2156) CpG site in the fifth CpG site (~ + 2156) 90%). Compared with the normal control group, the expression rates of CD4 ~ + CD25 ~ + T cells in the other two groups decreased significantly, with statistical significance (P <0.05). The expression of CD4 ~ + CD25 ~ + FOXP3 ~ + T cells in different groups were significantly different (P <0.01), diabetic nephropathy group was lower than the other two groups (P <0.05). The expression of CD4 ~ + CD25 ~ + FOXP3 ~ + T cells among the three groups showed a trend of decline with the aggravation of disease. Age, HbAlc, fasting blood glucose, leucocyte and diabetes duration were negatively correlated with the expression of CD4 ~ + CD25 ~ + FOXP3 ~ + T cells (P <0.05). Conclusions Down-regulation of FOXP3 promoter hypermethylation and CD4 ~ + CD25 ~ + FOXP3 ~ + T cell expression may be related to the pathogenesis of type 2 diabetic nephropathy.