绞股蓝皂苷降低2型糖尿病并非酒精性脂肪性肝病大鼠血糖、血脂的机理研究

The Mechanism of Blood Sugar,Triglycerides and Total Cholesterol Reduced by Gypenoside in Rats with Type 2 Diabetes Mellitus and Nonalcohol Fatty Liver Disease

目的:研究绞股蓝皂苷(Gypenosides,GPS)降低2型糖尿病(Type 2 diabetes Mellitus,T2DM)并非酒精性脂肪性肝病(nonalcohol fatty liver disease,NAFLD)大鼠血糖、血脂的机理。方法:65只SPF级雄性SD大鼠随机分为空白对照组(N组,n=7),NAFLD模型组(NM组,n=7),T2DM并NAFLD模型组(模型组,n=51)。分别建立NAFLD模型和T2DM并NAFLD大鼠模型。T2DM并NAFLD模型大鼠分别给予GPS[1 g/(kg.d)]干预(JH组,n=9),GPS[0.5 g/(kg.d)]干预(JL组,n=9),以纯净水灌胃作为对照(M组,n=9)。定量PCR技术检测肝组织过氧化物酶体增殖物激活受体γ(Peroxisome proliferator-activated receptorγ,PPARγ),检测血糖(Blood sugar,BS)、甘油三酯(Triglycerides,TG)、总胆固醇(Total cholesterol,TC)变化,肝组织切片HE染色观察肝脏病理学。结果:GPS干预显著降低T2DM并NAFLD模型大鼠BS、TG、TC,上调肝组织PPARγ表达水平,减轻肝脏脂肪浸润程度,并呈剂量依赖性。结论:GPS能降低T2DM并NAFLD大鼠BS、TG、TC,可能通过上调肝组织PPARγ表达干预BS、TG、TC代谢。

Objective To investigate the mechanism of blood sugar,triglycerides and total cholesterol reduced by gypenoside in rats with type 2 diabetes mellitus and nonalcohol fatty liver disease(NAFLD).Methods Sixty-five SPF male SD rats body weight 220 to 250 g,were randomly divided into blank control group(group N,n=7),NAFLD model group(group NM,n=7),NAFLD combined T2DM model group(n=51).The NAFLD model,NAFLD combined T2DM model of rats were prepared.The survival NAFLD combined T2DM model rats were further divided into group JH,group JL and group M(n=9).The rats of group JH were given gypenoside with a dose of 1 g/(kg·d),the rats of group JL were given gypenoside with a dose of 0.5 g/(kg·d),and the rats in group M were given distilled water.The changes of peroxisome proliferator-activated receptorγ(PPARγ),blood sugar(BS),triglycerides(TG),total cholesterol(TC) in liver tissue were determined by quantitative PCR.The pathological changes of liver tissue was observed with HE staining.Results The intervention of gypenoside significantly decreased the levels of BS,TG,TC in NAFLD combined T2DM model rats,up-regulated the expression of PPARγ,decreased the infiltration of liver fats in a dose-dependent manner.Conclusion Gypenoside could decrease the BS,TG,TC levels in NAFLD combined T2DM model rats through up-regulating the expression of PPARγ to interfere with their metabolism.