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目的探讨滋阴益气、补肾活血解毒法组方(降糖益肾方)对MKR转基因小鼠2型糖尿病肾病早期的保护作用。方法15周龄MKR鼠24只,根据性别和空腹血糖分层,随机分为3组,即模型组、中药组[降糖益肾方16.72g/(kg·d)]、西药组[格列喹酮4.33mg/(kg·d)+贝那普利1.44mg/(kg·d)],同期另设C57BL/6野生型小鼠为正常组。用药组分别给予相应剂量药物灌胃,模型组和正常组给予等容量蒸馏水灌胃。30d后,同步观察各组小鼠的空腹血糖、尿微量白蛋白和尿β2-微球蛋白(ELISA法)的含量,电镜观测肾脏病理改变。结果给药30d后,降糖益肾方能显著降低MKR鼠空腹血糖、尿微量白蛋白和尿β2-微球蛋白的排泄,与给药前比较,P<0.01;与模型组比较,P<0.01。电镜结果显示:降糖益肾方组肾小球基底膜增厚减轻,系膜区基质堆积减少。结论降糖益肾方能显著改善MKR鼠空腹血糖、降低尿微量白蛋白和尿β2-微球蛋白的含量、改善肾脏的病理损害,从而延缓MKR鼠肾脏病变的进一步发展。
Objective To explore the protective effects of Prescription of Nourishing Yin and Qi, Tonifying the Kidney and Promoting Blood Circulation to Deflate Toxins (type 2) on early type 2 diabetic nephropathy in MKR transgenic mice. Methods A total of 24 MKR rats aged 15 weeks were randomly divided into three groups according to sex and fasting glucose level: model group, Chinese medicine group (16.72g / (kg · d)], western medicine group 4.33 mg / (kg · d) of quinolone and 1.44 mg / (kg · d) of benazepril), while C57BL / 6 wild-type mice were set as the normal group in the same period. The treatment group were given the corresponding dose of drug gavage, model group and normal group given equal volume of distilled water gavage. After 30 days, the content of fasting blood glucose, urine microalbuminuria and urinary β2-microglobulin (ELISA) in each group were observed simultaneously. The pathological changes of kidney were observed by electron microscope. Results After 30 days of administration, Jiangtangyishen Decoction significantly reduced the fasting blood glucose, urinary microalbuminuria and urinary β2-microglobulin excretion in MKR rats, P <0.01 compared with those before administration; P < 0.01. Electron microscopy showed: Jiangtangyishen group glomerular basement membrane thickening reduced, the accumulation of mesangial matrix decreased. Conclusion Jiangtangyishen can significantly improve the fasting blood glucose in MKR mice, reduce the content of urinary microalbuminuria and urinary β2-microglobulin, and improve the renal pathological damage, thereby delaying the further development of renal lesions in MKR mice.