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目的探讨通络方剂对实验性糖尿病大鼠胸腺CD4+CD25+调节性T细胞(Treg)的影响。方法 112只SD大鼠随机分为3组:正常对照组、糖尿病模型组、通络方剂干预组。后两组一次性腹腔注射链脲佐菌素60mg/kg制备1型糖尿病大鼠模型。通络方剂干预组再分为2组:分别于糖尿病造模成功后当天及普通饲养12周后0.4g.kg-1.d-1)灌胃给药,即预防性给药组(TL-1)和治疗性给药组(TL-2)。灌胃时间均为12周。实验周期6个月,不同时间点(对照组和模型组:4、8、12、16、20、24周;通络方剂组:12和24周)处死大鼠,流式细胞仪检测胸腺CD4+CD25+Treg数量及其占CD4+T细胞比例,H-E染色观察胸腺形态,免疫组化检测Foxp3蛋白表达。结果随糖尿病病程发展,与正常对照组相比,糖尿病大鼠胸腺逐渐萎缩,Treg占CD4+T细胞比例逐渐减少,Foxp3表达减少。两组通络方剂组较糖尿病组Treg比例升高(P<0.01),胸腺指数升高(P<0.05),Foxp3有表达。结论通络方剂可显著提高Treg比例,提高胸腺指数,提高Foxp3表达,可能对实验性糖尿病大鼠的胸腺Treg有保护作用。
Objective To investigate the effect of Tongluo Prescription on CD4 + CD25 + regulatory T cells (Treg) in thymus of experimental diabetic rats. Methods One hundred and twelve SD rats were randomly divided into three groups: normal control group, diabetic model group and Tongluo Recipe intervention group. The latter two groups were given a single intraperitoneal injection of streptozotocin 60mg / kg rat model of type 1 diabetes. Tongluo Recipe intervention group was further divided into two groups: 0.4g.kg-1.d-1) were administered intragastrically after preventive diabetes mellitus (TL- 1) and therapeutic administration group (TL-2). Gavage time are 12 weeks. The experimental period was 6 months and the rats were sacrificed at different time points (control group and model group: 4, 8, 12, 16, 20 and 24 weeks; Tongluo recipe group: 12 and 24 weeks) + CD25 + Treg and its proportion of CD4 + T cells. The morphology of thymus was observed by HE staining and the expression of Foxp3 protein was detected by immunohistochemistry. Results Compared with the normal control group, the thymus of diabetic rats gradually decreased, the proportion of Tregs in CD4 + T cells decreased, and the expression of Foxp3 decreased. The ratio of Treg in two groups of Tongluo Prescription group was higher than that in diabetic group (P <0.01), the thymus index was increased (P <0.05), Foxp3 was expressed. Conclusion Tongluo Recipe can significantly increase the proportion of Treg, increase thymus index and increase Foxp3 expression, which may have protective effect on thymus Treg in experimental diabetic rats.