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灵芝多糖通过影响β细胞对链脲佐菌素诱导的糖尿病大鼠发挥降血糖作用。

Ganoderma lucidum polysaccharides exert anti-hyperglycemic effect on streptozotocin-induced diabetic rats through affecting β-cells.

作者信息

Zheng Jusheng, Yang Bin, Yu Yinghua, Chen Qi, Huang Tao, Li Duo

机构信息

Department of Food Science and Nutrition, Zhejiang University, Hangzhou, China.

出版信息

Comb Chem High Throughput Screen. 2012 Aug;15(7):542-50. doi: 10.2174/138620712801619168.

Abstract

Previous studies have demonstrated that Ganoderma lucidum polysaccharides (Gl-PS) exhibited potential antihyperglycemic effect in rats. The aim of the present study was to investigate the mechanism of the hypoglycemic effect of a low- molecular-weight Gl-PS in streptozotocin (STZ)-induced diabetic Sprague-Dawley (SD) rats. Gl-PS was extracted and purified from Ganodema lucidum fruiting body. 50 male SD rats were included in the study; 10 were taken as healthy controls; 40 were induced to diabetes by a single injection of 65 mg/kg STZ, of which 30 were selected as successful diabetic rat models. The 30 diabetic rats were divided into three groups: Gl-PS (200 mg/kg Gl-PS), metformin (100 mg/kg metformin) and diabetic control (n = 10 per group). After eight weeks' oral administration, plasma concentrations of fasting glucose, triacylglyceride, total cholesterol and nitric oxide were significantly decreased in Gl-PS and metformin groups. Pancreatic superoxide dismutase, catalase and glutathione peroxidase were significantly increased in Gl-PS and metformin groups. Histopathological results showed that Gl-PS and metformin had protective effect on β-cells. The mRNA expressions of Bcl-2 and PDX-1 in pancreas were up-regulated, but Bax, iNOS and Casp-3 down-regulated in Gl- PS and metformin groups compared to diabetic control group. The present results suggested that Gl-PS had a hypoglycemic effect in STZ-induced diabetic rats through preventing apoptosis of pancreatic β-cells and enhancing β-cells regeneration.

摘要

先前的研究表明,灵芝多糖(Gl-PS)在大鼠中显示出潜在的降血糖作用。本研究的目的是探讨低分子量Gl-PS对链脲佐菌素(STZ)诱导的糖尿病斯普拉格-道利(SD)大鼠降血糖作用的机制。从灵芝子实体中提取并纯化Gl-PS。该研究纳入了50只雄性SD大鼠;10只作为健康对照;40只通过单次注射65mg/kg STZ诱导糖尿病,其中30只被选为成功的糖尿病大鼠模型。30只糖尿病大鼠分为三组:Gl-PS组(200mg/kg Gl-PS)、二甲双胍组(100mg/kg二甲双胍)和糖尿病对照组(每组n = 10)。口服给药八周后,Gl-PS组和二甲双胍组的空腹血糖、甘油三酯、总胆固醇和一氧化氮血浆浓度显著降低。Gl-PS组和二甲双胍组的胰腺超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶显著增加。组织病理学结果显示,Gl-PS和二甲双胍对β细胞有保护作用。与糖尿病对照组相比,Gl-PS组和二甲双胍组胰腺中Bcl-2和PDX-1的mRNA表达上调,但Bax、iNOS和Casp-3下调。目前的结果表明,Gl-PS通过防止胰腺β细胞凋亡和增强β细胞再生,对STZ诱导的糖尿病大鼠具有降血糖作用。

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