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作 者:董柳[1] 甄仲[1] 李敏[1] 陈良[1] 赵昱[2] 段军[3] 潘琳[3] 仝小林[1]
机构地区:[1]中国中医科学院广安门医院,北京100053 [2]民航总医院,北京100123 [3]中日友好医院,北京100029
出 处:《辽宁中医药大学学报》2011年第11期42-45,共4页Journal of Liaoning University of Traditional Chinese Medicine
基 金:国家重点基础研究发展计划(973计划)资助项目(2010CB530600)
摘 要:目的:观察消膏转浊方对高脂饲养的肥胖大鼠肝脏TNF-α和瘦素与脂质过氧化反应的相关性。方法:Wister雄性SPF级大鼠40只。喂养1周后随机分为5组。正常组以标准饲料喂养;其余组的大鼠饲以高脂饲料。8周后,正常组饮食同前;模型组继续高脂喂养;消膏转浊组以及罗格列酮组改为普通饲料喂养,同时给予药物治疗,饮食控制组改为普通饲料喂养。共为12周。取材后检测肝匀浆中TNF-α、瘦素、FFA、MDA、SOD的含量;同时检测CYP2E1的蛋白及mRNA的表达。结果:与模型组相比,消膏转浊方能够显著地降低肝匀浆中TNF-α、FFA以及MDA的含量(P<0.01),瘦素(P<0.05),同时提高SOD的活性(P<0.01)。免疫组化定量分析以及实时荧光定量结果显示:与模型组相比,消膏转浊组肝细胞中CYP2E1染色阳性的细胞面积和MOD值显著低于模型组(P<0.01)同时CYP2E1 mRNA的表达显著低于模型组(P<0.01)。结论:消膏转浊方可以逆转肝脏细胞脂肪变性,其机制可能是通过降低肝脏TNF-α的过度表达改善瘦素抵抗进一步减少肝脏脂质过氧化反应来达到的。Objective:To Study on the correlations of the leptin and TNF-αwith the action of lipid peroxidation of fatty rats with Xiaogao Zhuanzhuo Preparation.Methods:Forty clean graded male Wister rats,ware fed 1W normally,then were randomly divided into 5 groups,The normal control group are fed with ordinary diet;the rest are fed with high fat diet.After 8W,the diet of the normal control group and the model group don’t change,and diet of the rest change to the ordinary food.At the same time,the rats of the rosiglitazone group and the Xiaogao Zhuanzhuo group are poured with drugs.At the end of twelve week of the experiment,we reckon TNF-α,Leptin,FFA,MDA and SOD in the liver homogenate.At the same time to observe the protein expression of CYP2E1 by immunohistochemistry and the mRNA expression of CYP2E1 by RT-PCR.Result:Compared with the model group,Xiaogao Zhuanzhuo preparation can decrease significantly the content of TNF-α,FFA,MDA and Leptin(P〈0.01,P〈0.05),but the activity of the SOD increased markedly(P〈0.01).Immunohistochemistry experiments display that the positive area and the MOD numerus of CYP2E1 decrease significantly(P〈0.01).RT-PCR experiments show that the expression of CYP2E1 mRNA decrease markedly(P〈0.01).Conclusion:Xiaogao Zhuanzhuo Preparation have the function of reduction the fat deposition in the hepatocyte.The mechanisms may be pass the decreasing the content of TNF-α and Leptin thereby ameliorating the action of lipid peroxidation.
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