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作 者:王雨[1] 郝洁[2] 李婕[3] 陈诚[1] 黄俊英[1] 黄河清[1,3]
机构地区:[1]中山大学药学院药理毒理实验室,广州510006 [2]郑州大学第一附属医院药学部,郑州450052 [3]中山大学实验动物中心,广州510006
出 处:《中药药理与临床》2016年第2期50-53,共4页Pharmacology and Clinics of Chinese Materia Medica
基 金:国家科技重大专项子课题(No:2014ZX09301307-008);教育部博士点基金(NO:20130171110097);广东省科技计划项目(NO:2014A020210007;2012B050300017)的资助
摘 要:目的:探讨虎杖苷通过Akt通路调节2型糖尿病(T2DM)大鼠糖脂代谢的作用机制。方法:本研究采用高脂高糖饮食加小剂量链脲菌素(STZ)联合诱导的2型糖尿病大鼠模型,观察灌胃给予虎杖苷(75 mg/kg、150 mg/kg)后对糖尿病大鼠血糖血脂、肝脏病理形态以及肝脏组织Akt、GSK3β、GCK、LDLR的影响。结果:虎杖苷在75 mg/kg给药剂量时就能有效调节2型糖尿病大鼠的糖脂紊乱,降低模型动物空腹血糖(FBG)、糖化血清蛋白(GSP)、糖化血红蛋白(Hb A1c)、胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)水平;减轻肝脏组织病理损伤,明显激活模型动物肝脏组织的Akt蛋白表达,进而促进下游GSK-3β的磷酸化,上调GCK,LDLR的蛋白表达,与150 mg/kg剂量组没有明显差异。结论:虎杖苷可以有效调节糖脂代谢且该作用与其影响Akt信号通路密切相关。Objective: To explore the role of polydatin on glucose and lipid metabolisms in type 2 diabetic rats involving the Akt signaling pathway.Methods: Diabetic rats were induced by a high-fat and high-sugar diet with low-dose streptozoin( STZ,30 mg / kg) and randomly divided into model,high dose of polydatin( 150 mg / kg),low dose of polydatin( 75 mg / kg) and pioglitazone( 5 mg / kg) treatment groups( n = 8).Another 8 normal rats were selected in control group. Each group was given the corresponding treatment for 8 weeks. The fasting blood glucose( FBG),glycosylated serum protein( GSP),glycosylated hemoglobin( Hb A1c),serum total cholesterol( TC),triglycerides( TG),low-density lipoprotein cholesterol( LDL-C),high-density lipoprotein cholesterol( HDL-C) were measured by the commercially available kits. H&E staining was made to analysis the histopathological changes in liver. Meanwhile,western blot assay was applied to detect the phosphorylation levels of Akt,glycogen synthase kinase-3β( GSK-3β) and protein expression of glucokinase( GCK) and low-density lipoprotein receptor( LDLR). Results: Polydatin( 75 mg / kg) can significantly attenuate the abnormal increase of FBG,GSP,Hb A1 c levels and improved level levels of TC,TG,LDL-C in type 2 diabetic rats( p 〈 0. 05). Furthermore,Polydatin( 75 mg / kg) can also protect the diabetic rats from pathological damage in liver and significantly increased phosphorylation levels of Akt and GSK-3β,then increased protein levels of GCK and LDLR in diabetic rat liver,which has no significant difference with the dosage of 150 mg / kg. Conclusion: Polydatin has obvious effect on regulating the glucose and lipid metabolisms in type 2 diabetic rats. The underlying mechanism was closely related to the Akt signaling pathway.
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