白介素-10表达上调介导脂氧素在急性肝损伤中的保护效应  

Up-Regulation of Interleukin-10 Mediates the Protective Effects of Lipoxin on Acute Liver Injury

作　　者：张力[1] 万敬员[2] 段红[1] 罗福玲[3] 代先坤[2] 

机构地区：[1]重庆医科大学病理生理学教研室,重庆市400016 [2]重庆医科大学药理学教研室,重庆市400016 [3]重庆医科大学附属第一医院药剂科,重庆市400016

出　　处：《医学分子生物学杂志》2008年第3期225-228,共4页Journal of Medical Molecular Biology

基　　金：国家自然科学基金(No.30570726)~~

摘　　要：目的研究脂氧素对四氯化碳诱导的肝损伤的保护作用与保护性细胞因子白介素-10的关系。方法小鼠腹腔注射四氯化碳诱导急性肝损伤。以脂氧素受体激动剂BML-1111mg/kg腹腔注射,或再应用抗-IL-10中和抗体后,取肝组织切片、HE染色观察肝细胞受损情况;收集血清检测转氨酶ALT和AST活性;RT-PCR检测肝组织中IL-10mRNA含量;ELISA检测血浆IL-10和TNF-α浓度。结果BML-111促进四氯化碳损伤的小鼠肝组织中IL-10mRNA表达、升高血浆IL-10浓度。抗-IL-10中和抗体可明显削弱BML-111对肝组织损伤及血清转氨酶水平的抑制作用,这一效应伴有血浆TNF-α浓度的升高。结论脂氧素受体激动剂BML-111可增强四氯化碳损伤的肝组织中白介素-10的表达,白介素-10是介导BML-111的保肝效应的重要细胞因子。Objective To investigate lipoxin on CCl4-induced liver damage and was injected into the peritoneum to induce the correlations between the hepatic protective effects of interleukin-10. Methods Carbon tetrachloride （ CCl4 ） acute liver injury and then BML-111 at 1 mg/kg was administrated. Then anti-IL-10 antibody was injected intraperitoneally. The hepatic damage was histologically examined by HE Staining. The serum aminotransferase （ALT and AST） was detemined. Hepatic IL-10 mRNA was detected by RT-PCR and the concentrations of IL-10 and TNF-α in the plasma were measured by ELISA. Results BML-111 promoted IL-10 mRNA expression in CCl4- injuried liver tissue and increased plasma IL-10 concentrations. Treatment of with anti-IL-10 antibody partially abolished the suppressive, effects of BML-111 on hepatic damage and the serum ALT and AST levels were elevated after CCl4 administration. The concentration of plasma TNF-α was also increased after IL-10 neutralization. Conclusion Lipoxin receptor agonist BML-111 plays a protective role in acute liver injury induced by CCl4, and this beneficial effect seems to be mediated through promoting IL-10 expression in CCl4-injuried liver.

关 键 词：脂氧素 四氯化碳 急性肝损伤 白细胞介素-10 

分 类 号：R364.5[医药卫生—病理学]