落新妇甙对肝缺血再灌注损伤细胞因子信号转导抑制分子1表达的影响  

Effect of astilbin on expression of supressors of cytokine signaling I in liver warm ischemia-reperfusion injury

作　　者：慕宁 江艺 杨芳 

机构地区：[1]解放军南京军区福州总院肝胆外科,福州350025

出　　处：《中华实验外科杂志》2014年第4期765-767,共3页Chinese Journal of Experimental Surgery

基　　金：福建省自然科学基金资助项目（2011Y0046）

摘　　要：目的观察落新妇甙对肝脏缺血再灌注损伤中对炎症信号通路的影响，探讨其缺血再灌注保护作用的分子机制。方法C57BL/6小鼠随机分为4组：假手术组（Sham）、模型组（I/R）、落新妇甙小剂量（10mg/kg）干预组和落新妇甙大剂量（40mg/kg）干预组。缺血前24h和1h干预组小鼠腹腔注射分别给予10mg/kg或40mg/kg落新妇甙，建立肝左、中叶70％部分肝缺血再灌注模型，模型组和假手术组给予同体积的生理盐水。小鼠肝脏左叶缺血90rain、再灌注6h后各实验组采集血液和肝脏组织样本。Western blot检测肝组织中细胞因子信号转导抑制分子1（SOCS-1）、白细胞介素（IL）-10蛋白含量，半定量逆转录一聚合酶链反应（SqRT-PCR）检测上述分子mRNA表达。结果落新妇甙小、大剂量干预组肝组织中SOCS-1、IL-10蛋白表达与I/R模型对照组比较均逐渐升高，与SqRT-PCR结果相符（P〈0．05）。结论落新妇甙干预能促进缺血再灌注损伤肝组织中IL-10蛋白及mRNA的高表达，从而起到抑制炎症的作用；落新妇甙干预能促进缺血再灌注损伤肝组织SOCS-1蛋白和mRNA的表达，显示其可能通过上调SOCS-1负调节通路，产生抑制炎症的作用。Objective To study the molecular mechanism of the effect of astilbin on the anti-in- flammation signaling pathway in liver warm ischemia-reperfusion injury. Methods C57BL/6 mice were randomly divided into four groups （ n = 5 ） ： sham-operated group （ Sham ）, model control group （ I/R ）, low dosage of astilbin treatment group （10 mg/kg） and high dosage of astilbin （40 mg/kg） treatment group. Twenty-four h and one h before Isehemia, the mice in the treatment groups were intraperitoneally in- jected with 10 or 40 mg/kg astilbin. Then the hepatic ischemia-reperfusion model of 70 percent of liver, including the left and middle hepatic lobes, was established. The I/R model control group and the sham operated group were administered with the same volume of normal saline. After 90 rain isehemia and 6 h reperfusion of the partial hepatic lobe, liver tissue samples were collected from the experimental groups. The contents of supressors of cytokine signaling 1 （ SOCS-1 ） and interleukin （IL） -10 in liver tissues were detected by using Western blotting. The mRNA expression of the same proteins was detected by using semi- quantitative reverse transcriptase-polymerase chain reaction （SqRT-PCR）. Results As compared with the I/R model control group, SOCS-1 and IL-10 protein levels were gradually increased in treatment groups, and higher in the high dosage group than in the low dosage group. The result of mRNA expression showed a same trend （ P 〈 0. 05 for low dosage group ; P 〈 0. 01 for high dosage group）. Conclusion Intervention with astilbin can promote the expression of IL-10 protein and mRNA in IRI liver, thus inhibiting the inflam mation; Intervention with astilbin can promote the expression of SOCS-I protein and mRNA in IRI liver, showing its role of negative regulation by upregulating SOCS-1 pathway.

关 键 词：落新妇甙 肝缺血 再灌注损伤 白细胞介素-10 细胞因子信号转导抑制分子1 

分 类 号：R363[医药卫生—病理学]