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机构地区:[1]浙江中医药大学 [2]浙江中医药大学附属第一医院消化病研究室
出 处:《中西医结合肝病杂志》2009年第3期161-164,I0001,共5页Chinese Journal of Integrated Traditional and Western Medicine on Liver Diseases
基 金:浙江省卫生厅资助项目(No.2007YA009)
摘 要:目的:观察酒精性肝病形成中大鼠血清瘦素水平、肝组织瘦素及其受体表达的动态变化,探讨瘦素及其受体在酒精性肝病形成中的发病机制。方法:SD雄性大鼠随机分为正常组和模型组,以白酒-玉米油-吡唑混合液灌胃建立酒精性肝病动物模型,分别在4、8、14周末光镜观察大鼠肝脏组织学变化情况,免疫组化法检测肝组织瘦素及其受体的表达,ELISA法检测大鼠血清瘦素水平。结果:模型组大鼠肝组织在4周时出现轻度脂肪变及腺泡内个别点状坏死灶,8周时脂肪变程度加重、腺泡内点状坏死灶增多、门管区炎细胞浸润,14周脂肪变和炎症程度进一步加重;模型组大鼠4周时,肝组织瘦素及其受体表达、血清瘦素水平与同期正常组比差异无显著性意义(P>0.05),随着肝脏损伤程度的加重,三者均明显增加(P<0.05,P<0.01);肝组织中瘦素及其受体表达水平与肝脏脂肪变及炎症程度均呈明显正相关。结论:在白酒-玉米油-吡唑混合液灌服复制的大鼠酒精性肝病形成过程中,瘦素及其受体表达增加,且随肝脏损伤程度的加重而逐渐增加,提示其参与了酒精性肝病的发生发展。Objective: To investigate the dynamic changes of the levels of serum leptin, expression of leptin and its receptor in hepatic tissue during the process of forming alcoholic liver disease in rats. To explore the etiopathogenesis of leptin and its receptor in alcoholic liver disease. Methods: SD male rats were randomly divided into normal group and model group. The model of alcoholic liver disease in rats could be established by dealing with the mixture of alcohol, corn oil, and pyrozole. The changes of hepatic histology were assessed by microscopic examination at the end of 4th, 8th, 14th week. Expression of leptin and its receptor in hepatic tissue was detected by immunohistochemistry. Levels of serum leptin were detected by ELISA. Results : Hepatic tissue of model group showed slightly steatosis and punctual putrescence in acinus at the end of 4th week ; and at the end of 8th week, the steatosis of liver tissue was gradually serious, more punctual putrescence in acinus and the inflammatory cells infiltrated in portal area can be found; at the end of 14th week, the degrees of steatosis and inflammation were further severe. The expression of leptin and its receptor in hepatic tissue and the levels of serum leptin had not remarkable difference at the end of 4th week in the model group rats ( P 〉 0. 05 ) . Along with the aggravation of liver injury, all the indicators increased significantly ( P 〈 0. 05, P 〈 0. 01 ) . The expressions of leptin and its receptor in hepatic tissue were positively correlated with the degrees of liver steatosis and inflammation. Conclusion: In the process of forming alcoholic liver disease induced by dealing with alcohol, corn oil, and pyrozole in rats, expression of leptin and its receptor were elevated and correlated with stage of liver injury positively, which shows that leptin and its receptor may be concerned with the development of alcoholic liver disease.
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