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作 者:王荣琦[1] 南月敏[1] 赵素贤[1] 米红梅[1] 孔令波[1] 贾彦红[1]
机构地区:[1]河北医科大学第三医院中西医结合肝病科,050051
出 处:《肝脏》2011年第3期216-219,共4页Chinese Hepatology
摘 要:目的观察壳脂胶囊对小鼠非酒精性脂肪性肝炎(NASH)肝组织氧化应激及脂质过氧化反应的影响,探讨其对NASH的防治作用及机制。方法健康雄性C57BL/6J小鼠18只,随机分为三组,每组6只。采用高脂、胆碱-蛋氨酸缺乏(MCD)饮食4周建立小鼠NASH模型,应用壳脂胶囊进行干预实验,并以胆碱-蛋氨酸充足饮食设立对照组。光镜下观察肝组织脂肪变性及炎症反应程度;硫代巴比妥酸法测定肝组织丙二醛(MDA)含量,比色法测定超氧化物歧化酶(SOD)活性;实时定量PCR检测肝脏血红素氧合酶-1(HO-1)和细胞色素P4502E1(CYP2E1)mRNA的表达。结果对照组小鼠肝脏未出现明显的脂肪变及炎症;模型组小鼠肝组织脂肪变性及炎症明显,MDA水平显著增高(P<0.001),SOD活性明显降低(P<0.01),HO-1和CYP2E1的表达显著升高(P<0.001,P<0.01);壳脂胶囊干预组肝组织脂肪变性及炎症均较模型组明显减轻,MDA水平显著下降(P<0.01),SOD活性明显增强(P<0.05),HO-1及CYP2E1表达明显降低(P<0.05)。结论壳脂胶囊可降低饮食诱导的小鼠NASH肝组织HO-1、CYP2E1表达,减轻氧化应激和脂质过氧化反应,阻止NASH的发生、发展。Objective To elucidate the effect and the mechanism of Kezhi capsule on the oxidative stress and lipid peroxidation in mice with nutritional steatohepatitis.Methods C57BL/6J mice were fed with methionine-choline deficient(MCD) diet for 4 weeks to induce hepatic steatohepatitis.Kezhi capsule solution(0.7 g/kg)was administered to mice by daily intragastric gavag.HE and Sudan Ⅳ stain were used for the observation of steatosis,inflammatory response in liver sections.Thiobarbituric acid reactive substances analyzed malondialdehyde(MDA) content;colorimetry detected superoxide dismutase(SOD) activity and real-time polymerase chain reaction detected the mRNA expressions of heme oxygenase-1(HO-1) and cytochrome P4502E1(CYP2E1).Results Compared with those in control groups,mice fed with the MCD diet developed steatohepatitis with hepatocyte ballooning changes,scattered lobular inflammatory cells infiltration,and inflammatory foci.Hepatic contents of MDA increased markedly(P0.001),anti-oxide SOD activity decreased significantly(P0.01) and the gene expressions of HO-1 and CYP2E1 were up-regulated dramatically(P0.001,P0.01).Compared with those in MCD group,the hepatic pathological changes and oxidative stress injury were ameliorated,the messenger RNA expressions of HO-1 and CYP2E1 were down-regulated obviously in Kezhi capsule group(P0.05).Conclusion Kezhi capsule can interrupt the progression of nutritional steaohepatitis by suppressing the expressions of HO-1 and CYP2E1,attenuating hepatic oxidative stress and lipid peroxidation,which will provide new insight into treatment of steatohepatitis.
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