T-2毒素对于猪肝细胞毒性的分子机制研究  

The Molecular Mechanism of T-2 Toxin-induced Toxicity in Liver Cell of Pig

作　　者：王敏辉[1] 李吕木[1,2] 钱坤 许发芝[1,2] 丁小玲[1,2] 刘海进[1] 

机构地区：[1]安徽农业大学动物科技学院,安徽合肥230036 [2]安徽省畜牧生物工程技术研究中心,安徽合肥230031

出　　处：《激光生物学报》2011年第5期639-644,共6页Acta Laser Biology Sinica

基　　金：国家"973"计划项目(2009CB118800)

摘　　要：为了探讨T-2毒素对于家畜的毒性机理及诱导凋亡的分子机制,用T-2毒素对猪的肝脏细胞进行暴露,暴露浓度分别为0、0.02mg/L、0.05mg/L、0.1mg/L,暴露时间为48h,然后用微阵列技术检测0.05mg/L处理组基因表达谱的变化。结果表明,氧化应激和细胞凋亡相关基因发生上调,药物和脂质代谢的基因发生下调,同时荧光定量PCR对细胞色素P450家族的CYP2D25和CYP51两个药物代谢基因的表达情况进行了进一步的验证。结果表明,T-2毒素对猪肝细胞的毒性机制可能是引起丝裂原活化蛋白激酶(MAPK)途径氧化应激,进而导致细胞凋亡。To determine the molecular targets and toxicity mechanisms of T-2 toxin induced apoptosis in liver cell of pig. The liver cell of pig were treated with 0,0.02 mg/L,0.05 mg/L,0.1 mg/L of T-2 toxin for 48 b. To examine the gene expression profiles, the live treated with 0.05 mg/L of T-2 toxin were performed with microarray analysis. Increased expression of oxidative stress and apoptosis-related genes were detected in the liver of pig, and decreased expres- sion of lipid metabolism- and drugmetabolizing enzyme-related genes were also detected in live tissues. The real-time RT-PCR also confirmed the decreased expression of CYP2D25 and CYP51 in the liver of pig. The results suggested that the mechanism of T-2 toxin-induced toxicity in pig may be due to oxidative stress followed by the activation of the mitogen-aetivated protein kinase （MAPK） pathway, finally inducing apoptosis.

关 键 词：T-2毒素 猪 肝脏细胞 凋亡 微阵列 

分 类 号：S828[农业科学—畜牧学]