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作 者:黄晓飞[1] 卢锟刚[1] 宋成武[1] 陈桂林[1] 余尚工[1] 方念伯[1]
机构地区:[1]湖北中医药大学中药资源与中药复方教育部重点实验室,武汉430065
出 处:《数理医药学杂志》2013年第2期197-200,共4页Journal of Mathematical Medicine
基 金:湖北大顶山制药有限公司降脂胶囊委托开发项目
摘 要:目的:研究复方绞股蓝软胶囊降血脂作用机制。方法:采用高脂饲料喂养雄性昆明种小鼠4w,复制实验性高脂血症小鼠模型。连续灌胃复方绞股蓝软胶囊内容物(剂量为345mg.kg-1.d-1)4w,测定小鼠血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白-胆固醇(HDL-C)的含量。同时采用逆转录-聚合酶链式反应技术(RT-PCR)检测肝脏中与脂代谢相关基因:载脂蛋白AI(ApoAI)、胆固醇7α-羟化酶(Cyp7α1)、3-羟-3-甲基戊二酸单酰辅酶A还原酶(Hmgcr)及固醇调控元件结合转录因子2(Srebf2)mR-NA的相对表达量。并对肝、肾、脾等脏器进行病理学检查。结果:与高脂模型组相比较,复方给药组小鼠血清TC、TG含量显著性降低(P<0.01),HDL-C含量显著性升高(P<0.01),小鼠肝脏病变情况较高脂模型组显著性好转。同时小鼠肝脏中ApoAI、Cyp7α1基因mRNA相对表达量显著性上调(P<0.01)、Hmgcr及Srebf2基因mRNA的相对表达量显著下调(P<0.01)。结论:复方绞股蓝软胶囊具有较好的降血脂作用,其降血脂作用机制是对肝脏中与脂代谢相关基因ApoAI、Cyp7α1、Hmgcr及Srebf2的表达调控有关。Objective: To investigate the mechanism of compound Gynostemma pentaphyllum soft capsule(CGS) for hypolipidemic effects.Methods: Hyperlipidemia mice model was established with a high-fat diet for 4 weeks.Then the compound group mice was given CGS(345mg·kg-1·d-1) intragastrically for 4 weeks consecutive days.The effects of CGS on serum levels of total cholesterol(TC),triglyceride(TG),high density lipoprotein cholesterol(HDL-C) were measured respectively,as well as the detection of liver apolipoprotein AI(ApoAI),3-hydroxy-3-methylglutaryl coenzyme A reductase(Hmgcr),cholesterol 7α1-hydroxylase(Cyp7α1),sterol regulatory element binding transcription factor 2(Srebf2) mRNA expressions was performed by reverse transcriptase polymerase chain reaction(RT-PCR).The pathological changes of liver tissues stained with Hematoxylin-eosin(HE) were observed under light microscope.Results: Compared with the hyperlipidemia model group mice,the CGS could significantly decreased the level of serum TC,TG and remarkably increased the concentration of serum HDL-C in the hyperlipemia mice(P0.01),and it had significantly effect on up-regulation of ApoAI and Cyp7α1 mRNAs,down-regulation of Hmgcr and Srebf2 mRNAs(P0.01).Conclusion: The CGS showed potent hypolipidemic effect,and the mechanism of hypolipidemic effect was probably regulation the mRNAs expression of four key cholesterol metabolism genes in liver.
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