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目的 :观察二甲双胍对2型糖尿病模型大鼠尿nephrin(UNE)排泄的动态影响,探讨二甲双胍对糖尿病肾小球足细胞的保护作用。方法:将高脂膳食联合小剂量链脲佐菌素(streptozotocin,STZ)诱导的2型糖尿病大鼠随机分为3组:糖尿病模型组、二甲双胍干预组、优降糖干预组,并设正常对照组。干预前后监测血糖(BG)以及尿白蛋白(UALB)和尿nephrin排泄、8周末糖化血红蛋白(Hb A1c)的变化。结果:13组糖尿病大鼠BG及Hb A1c均明显高于正常组(P<0.05);经二甲双胍和优降糖干预后,4、8周末2组BG和Hb A1c均明显低于2型糖尿病模型组(P<0.05),但差异无统计学意义(P>0.05);24、8周末各糖尿病大鼠尿白蛋白/肌酐比(UACR)明显高于正常组(P<0.05);与2型糖尿病模型组比较,二甲双胍和优降糖组UACR值明显降低(P<0.05),4周末,两干预组间无显著性差异(P>0.05),8周末,两组间差异有统计学意义(P<0.05);30、2周末,4组大鼠尿nephrin/肌酐比(UNER)差异无统计学意义,4、8周末,各糖尿病大鼠UNER均明显高于正常组(P<0.05),二甲双胍和优降糖干预组UNER明显低于糖尿病模型组(P<0.05),且二甲双胍组低于优降糖组(P<0.05);4Pearson相关分析显示UNER与UACR存在正相关(r=0.846,P<0.05)。结论 :二甲双胍可以降低糖尿病肾病大鼠尿nephrin的排泄,提示对肾小球足细胞可能存在保护作用,该作用不完全依赖于血糖的降低。
AIM: To observe the dynamic effects of metformin on excretion of urinary nephrin (UNE) in type 2 diabetic rats and to explore the protective effect of metformin on diabetic glomerulus podocytes. Methods: Type 2 diabetic rats induced by high fat diet combined with low dose streptozotocin (STZ) were randomly divided into three groups: diabetic model group, metformin intervention group, and glibenclamide intervention group, and normal control group. Blood glucose (BG), urinary albuminuria (UALB) and urine nephrin excretion were monitored before and after intervention, and the changes of HbA1c at 8weeks were monitored. Results: The levels of BG and Hb A1c in 13 diabetic rats were significantly higher than those in normal rats (P <0.05). After metformin and oral hypoglycemic intervention, the levels of BG and Hb A1c in 2 groups were significantly lower than those in type 2 diabetic rats (P <0.05), but the difference was not statistically significant (P> 0.05). Urine albumin / creatinine ratio (UACR) of diabetic rats at 24 and 8 weeks was significantly higher than that of normal rats (P <0.05) Diabetes mellitus group, metformin and glibenclamide group UACR decreased significantly (P <0.05), at the end of 4 weeks, there was no significant difference between the two intervention groups (P> 0.05), 8 weeks, the difference between the two groups was statistically significant P <0.05). There was no significant difference in urine nephrin / creatinine ratio (UNER) between the two groups at the end of the two weeks at the end of the two weeks. At the end of the 4th and the eighth week, the UNER in all diabetic rats was significantly higher than that in the normal group (P <0.05) The UNER of metformin and hyperglycemia intervention groups were significantly lower than those of diabetic model group (P <0.05), and the metformin group was lower than that of the hypoglycemic group (P <0.05); 4 Pearson correlation analysis showed that there was a positive correlation between UNER and UACR (r = 0.846, P <0.05). Conclusion: Metformin can reduce urinary nephrin excretion in diabetic nephropathy rats, suggesting that there may be a protective effect on glomerular podocytes, which is not completely dependent on the decrease of blood glucose.