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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(P<0.05);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(P<0.05)。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。
Objective: To investigate the effect of Gynostemma Pentaphyllum polysaccharide on renal function in diabetic rats and its possible mechanism of protection. Methods: Type 2 diabetes model was established by intraperitoneal injection of streptozotocin (STZ) in rats with high-fat, high-sugar diet. The gavage of Gynostemma pentaphyllum was given for 8 weeks. The fasting blood glucose (FBG), serum creatinine, serum urea nitrogen, 24 h urine volume and urinary protein in rats were determined. The histopathological sections were observed for renal morphology and glomerular volume. Western blot The renal cortex NF-κB expression was detected. Results: Gynostemma pentaphyllum polysaccharide (GPS) could reduce FBG, serum creatinine, urine output and proteinuria in DN group in a dose-dependent manner, but there was no significant difference between blood urea nitrogen model group and GPS group. After middle and high dose GPS treatment (P <0.05). Compared with model group (149.8 ± 12.2%), high dose of GPS could inhibit glomerular hypertrophy to 108.9 ± 9.6%. Further study found that GPS could decrease the expression of NF-κB protein in kidney of DN group in a dose-dependent manner. The level of NF-κB in high-dose and middle-dose groups was significantly lower than that in model group (P <0.05). Conclusion: Gynostemma polysaccharide has a protective effect on experimental diabetic nephropathy, which may be related to the inhibition of the expression of NF-κB in renal inflammation-related pathways.