绞股蓝多糖对糖尿病肾病大鼠肾功能的保护作用及其机制研究

目的:探讨绞股蓝多糖对糖尿病大鼠肾功能的影响及其保护的可能机制。方法:采用大鼠高脂高糖饲料结合腹腔注射链脲佐菌素建立2型糖尿病模型。灌胃给予绞股蓝多糖8周后,测定大鼠空腹血糖(FBG),血清肌酐、血清尿素氮、24 h尿量及尿蛋白等指标;组织病理切片观察肾形态,肾小球体积;Western blot法检测肾皮质NF-κB的表达。结果:绞股蓝多糖(GPS)可剂量依赖性的降低DN组的FBG、血肌酐、24 h尿量和尿蛋白;但血尿素氮模型组与GPS组无统计学差异;中、高剂量GPS治疗后,肾脏指数较模型组明显降低(P0.05);与模型组(149.8±12.2%)比较,高剂量GPS可抑制肾小球体积肥大至108.9±9.6%。进一步研究发现,GPS可剂量依赖性的降低DN组肾脏NF-κB蛋白的表达,高、中剂量组水平与模型组相比有统计学差异(P0.05)。结论:绞股蓝多糖对实验性糖尿病肾病具有保护作用,其机制可能与抑制肾炎症相关通路NF-κB的表达有关。

Protection of Renal Function by the Polysaccharide fromGynostemma pentaphyllumon Diabetic Nephropathy and Its Mechanism

Objective:To investigate the protective effects of polysaccharide from Gynostemma pentaphyllum on type 2 diabetic nephropathy and discuss the mechanisms.Methods:Diabetes rat model was induced by injection of streptozotocin after feeding high-fat and high-sugar diet. The rats were divided into six groups. After the rats were treated with Gynostemma pentaphyllum polysaccharide or positive control agent, enalapril for 8 weeks, the changes of fasting blood glucose (FBG), 24 h urine, urine protein and other biological indexes were assessed. The pathological changes in the kidney were determined by H&E staining. The expression of NF-kB was detected by western blotting.Results:Compared with model group, administration of the polysaccharide from Gynostemma pentaphyllum (GPS) can reduce FBG, plasma creatinine, 24 h urinary volume and urine protein in a dose-dependent manner. But there was no significant difference in blood urea nitrogen between model and GPS groups. After the 8-week treatment with medium or high dose of GPS, the kidney index was significantly decreased. High dose of GPS can decrease the glomerulus volume to 108.9 ± 9.6%, compared to the value of 149.8 ± 12.2% in model group. Furthermore,the expression of NF-kB protein in renal tissues was also significantly decreased.Conclusion:These data indicate that Gynostemma pentaphyllum polysaccharide protects renal function in rats of type 2 diabetes. The mechanismmay be related with the inhibition of inflammation via NF-kB signaling pathway.