落新妇甙对热缺血再灌注损伤肝脏肿瘤坏死因子α与白细胞介素-10表达的影响

Effects of astilbin on the expression of TNF a and IL-10 in liver warm ischemia-reperfusion injury

目的 观察落新妇甙对热缺血再灌注（I/R）损伤肝脏Th1、Th2型细胞因子表达的影响. 方法 C57BL/6小鼠随机分为4组：假手术组、模型组,落新妇甙小剂量（10 mg/kg）干预组和大剂量（40mg,/kg）干预组.干预组小鼠于缺血前24h和1 h分别给予10mg/kg或40mg/kg的落新妇甙腹腔注射,建立70%部分肝I/R模型.收集肝组织标本,Western blot检测肝组织中肿瘤坏死因子（TNF）α,白细胞介素（IL）-10蛋白含量,RT-PCR检测肝组织TNF α、IL-10 mRNA的水平.多组间比较采用单因素方差分析,两两比较采用SNK法.结果 与I/R模型对照组比较,小、大剂量落新妇甙干预组肝组织中TNF α蛋白表达水平依次降低,与TNF α mRNA的半定量RT-PCR结果 相符（相对表达量分别为1.74±O.12与1.56±0.09、0.82±0.12,P值均〈0.05） 而IL-10蛋白表达水平依次升高,与IL-10 mRNA的半定量RT-PCR结果 相符（相对表达量分别为0.96±0.08与1.11±0.17、1.47±0.08,P值均〈0.05）.结论 落新妇甙干预能抑制I/R损伤肝组织中Th1型细胞因子TNFα的高表达,同时促进Th2型细胞因子IL-10的表达.

Objective To investigate the effects of astilbin on the expressions of TNF α and IL-10 during liver warm ischemia-reperfusion injury. Methods C57BL/ 6 mice were randomly divided into 4 groups （n = 8）： 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. The treatment group mice were intraperitoneally injected with 10 or 40 mg/kg astilbin 24 hours and one hour before Ischemia, the hepatic ischemia-reperfusion model were thus established. After jn90 of min ischemia and 6 h reperfusion of the partial hepatic lobe, the expressions of TNF α and IL-10 in liver tissues collected from the experimental groups were detected by Western blot and semiquantitative RT-PCR. Results The expression of TNF a protein in liver tissues gradually decreased in treatment groups （low and high dosages of astilbin treatment groups） as compared to the I/R model control group. Similar results were observed in the mRNA expressions of these genes as determined by semiquantitative RT-PCR （P 〈 0.05 for low dosage group P 〈 0.01 for high dosage group）. Compared with the I/R model control group, the expression of IL-10 was increased in both treatment groups （low dosage group P 〈 0.05 large dosage group P 〈 0.01）. Conclusion Treatment with astilbin decreases TNF α expression but induces IL-10 expression in liver during warm ischemia-reperfusion injury.