糖复康对糖尿病大鼠肾皮质蛋白质非酶糖化的影响

Effect of Tangfukang on Nonenzymatic Glycosylation of Renal Cortex Protein in Early Diabetes Rats

关键词:  糖尿病肾病  非酶糖化  糖复康  氨基胍

Key words:  Diabetic nephropathy  Nonenzymatic glycosylation  Tangfukang  Aminoguanidin

摘要:

目的:研究中药糖复康对早期糖尿病大鼠肾皮质蛋白质非酶糖化的影响。方法:以氨基胍为对照药,对STZ糖尿病大鼠肾皮质糖化终产物(AGEs)、IV型胶原(IV-C)、纤维连接蛋白(FN)进行免疫组织化学研究。结果:模型糖尿病大鼠血糖明显升高,尿蛋白排泄率(UPR)增加,符合早期糖尿病诊断。糖复康、氨基胍均明显降低了UPR、肾皮质AGEs,与模型组比较差异均十分显着,且两者效果相当,糖复康还显着降低了肾皮质IV-C、FN积聚,与模型组比较差异十分显着(P<0.001),显着优于氨基胍组。结论:中药糖复康降低了糖尿病肾病大鼠肾皮质AGEs表达,表明抑制蛋白质非酶糖化是糖复康治疗糖尿病肾病(DN)的重要机理之一,而且不以降糖为条件。

Abstract:

Objective: To research the effect of Tangfukang, Chinese patent medicine, on renal cortex protein nonenzymatic glycosylation of early diabetes rats. Methods: AGEs, IV-C, and FN in STZ diabetes rats were studied with immunohistochemical technique using aminoguanidin as control. Results: Both sugar and UTP in STZ diabetes rats were increased, which coincided with the diagnosis of early diabetes. Tangfukang and aminoguanidin obviously decreased UTP and AGEs compared with model group. The effect of Tangfukang and aminoguanidin were similar. In addition, Tangfukang obviously decreased the accumulation of renal cortex IV-C and FN than that in model group and aminoguanidin. Conclusion: Tangfukang down-regulated the expression of renal cortex AGEs in diabetic rats with nephropathy (DN) without decreasing blood sugar. The depression of protein nonenzymatic glycosylation may be one of the important mechanisms of Tangfukang to prevent and cure DN.