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目的探讨非酶糖化与糖尿病肾病(DN)发生发展的关系以及非酶糖化抑制剂对DN的治疗作用。方法雄性Wistar大鼠40只,随机取10只为正常对照组,糖尿病组、糖尿病氨基胍[100mg/(kg·d)]治疗组、糖尿病黄芩苷[150mg/(kg·d)]治疗组,其余30只腹腔注射链脲佐菌素(60mg/kg)诱发糖尿病,随机分为16周后,处死大鼠,分离肾脏,测定组织非酶糖化,观察Bcl-2、Bax的表达,取部分肾皮质病理观察、电镜观察细胞凋亡的形态学变化。结果糖尿病组肾脏皮质非酶糖化高于对照组(P<0.001),氨基胍治疗组[(139.18±36.41)AUF/mg]、黄芩苷治疗组[(135.12±44.32)AUF/mg]非酶糖化低于糖尿病组[(251.09±51.74)AUF/mg],差别有统计学意义(P<0.01),而血糖无明显变化。糖尿病组肾脏Bcl-2蛋白表达减少、Bax蛋白表达增加,氨基胍治疗组、黄芩苷治疗组的Bcl-2蛋白表达比糖尿病组增多,而Bax蛋白表达比糖尿病组减少。透射电镜下见糖尿病组肾脏肾小管上皮细胞呈典型的凋亡形态学改变,氨基胍治疗组、黄芩苷治疗组大鼠肾组织细胞凋亡改变明显减轻。糖尿病组肾小球基底膜增厚,系膜区域扩大,治疗组病变减轻。结论非酶糖化抑制剂氨基胍、黄芩苷通过抑制非酶糖化,调节Bax、Bcl-2的表达,抑制细胞凋亡,明显改善糖尿病大鼠肾脏结构与功能,延缓DN的发展。
Objective To investigate the relationship between non-enzymatic glycation and the development of diabetic nephropathy (DN) and the therapeutic effect of non-enzymatic glycation inhibitors on DN. Methods Forty male Wistar rats were randomly divided into normal control group, diabetic group, diabetic aminoguanidine (100mg / (kg · d)] and diabetic baicalin [150mg / (kg · d) The other 30 rats were injected intraperitoneally with streptozotocin (60mg / kg) to induce diabetes. After randomly divided into 16 weeks, the rats were sacrificed and the kidneys were separated. The non-enzymatic glycation of tissues was measured. The expression of Bcl-2 and Bax was observed. Cortical pathological observation, electron microscopy morphological changes of apoptosis. Results The non-enzymatic glycation of renal cortex in diabetic group was significantly higher than that in the control group (P <0.001), while the aminoguanidine treatment group [(139.18 ± 36.41) AUF / mg] and the baicalin treatment group (135.12 ± 44.32 AUF / Lower than that in diabetic group [(251.09 ± 51.74) AUF / mg], the difference was statistically significant (P <0.01), but no significant change in blood glucose. Compared with diabetic group, the expression of Bcl-2 protein and Bax protein were increased in diabetic group and the expression of Bcl-2 protein in aminoguanidine group and baicalin treatment group was higher than that in diabetic group and Bax protein in diabetic group. The morphological changes of renal tubular epithelial cells in diabetic group were observed under transmission electron microscope. The apoptosis of renal tubular cells in aminoguanidine-treated group and baicalin-treated group was significantly reduced. Diabetic group glomerular basement membrane thickening, mesangial area expanded, the treatment group lesions reduced. Conclusions Aminoguanidine and baicalin, which are non - enzymatic glycation inhibitors, can inhibit the apoptosis and the renal structure and function of diabetic rats and retard the development of DN by inhibiting the non - enzymatic glycation, regulating the expressions of Bax and Bcl - 2.