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目的:探讨魔芋葡甘聚糖(GMN)防治链脲霉素(STZ)所致大鼠糖尿病的作用及机制。方法:于Wistar 大鼠腹腔注射50 mg·kg-1体重链脲霉素,建立糖尿病模型。分别于模型建立前后灌胃给予相同剂量的GMN,以血糖和尿糖及胰腺病理组织学检查为观察指标,同时检测肝匀浆超氧化物岐化酶(SOD)活性和过氧化脂质(LPO)含量以及血清淋巴因子IL-1 和TNF a水平。结果:GMN于模型建立前给药可明显降低糖尿病大鼠的血糖和尿糖值,停药后该作用可持续1 周时间。与模型对照组相比,病理切片显示胰岛仅有少量的炎性细胞浸润,无明显的β细胞损伤。GMN预防给药可增高SOD活性,减少LPO含量,但对细胞因子无明显作用。结论:GMN预防给药可防止STZ诱导的大鼠糖尿病发生,作用持久,降糖作用与清除体内自由基从而减少β细胞损伤有一定相关性。
Objective: To investigate the effect and mechanism of Konjac glucomannan (GMN) on the prevention and treatment of streptozotocin (STZ) -induced diabetes in rats. Methods: Wistar rats were injected intraperitoneally with 50 mg · kg -1 body weight streptozotocin to establish diabetic model. GMN with the same dose was given intragastrically before and after the model was established. Blood glucose and urine glucose as well as pancreatic histopathological examination were used as indexes to observe the activity of superoxide dismutase (SOD) and lipid peroxidation (LPO) ) Content and serum levels of IL-1 and TNF a. Results: Before administration of GMN, the blood glucose and urine glucose of diabetic rats were significantly decreased, and the effect of GMN could be sustained for one week after withdrawal. Compared with the model control group, the pathological sections showed that there was only a small amount of inflammatory cell infiltration in pancreatic islets without significant β-cell injury. GMN prophylaxis can increase SOD activity, reduce LPO content, but no significant effect on cytokines. CONCLUSION: GMN prophylaxis can prevent STZ-induced diabetic rats and prolong the duration of diabetes. Hypoglycemic effect may be related to clearance of free radicals in vivo and reduction of β-cell injury.