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T-2 toxin-induced apoptosis involving Fas,p53,Bcl-xL,Bcl-2,Bax and caspase-3 signaling pathways in human chondrocytes

查看全文 作  者:Jing-hong CHEN Jun-ling CAO Yong-lie CHU Zhi-lun WANG Zhan-tian YANG Hong-lin [1]WANG 高影响力作者 机构地区:[1]Ministry of Education Key Laboratory of Environment and Genes related to Diseases, Institute of Endemic Diseases, School of Medicine, Xi 'an Jiaotong University, Xi 'an 710061, China高影响力机构 出  处:《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》索引2008年第9卷第6期,共9页高影响力期刊 基  金:Project(Nos.3063058 and 30471499)supported by the National Natural Science Foundation of China 摘  要:Objective:To investigate the effects of T-2 toxin on expressions of Fas,p53,Bcl-xL,Bcl-2,Bax and caspase-3 on human chondrocytes.Methods:Human chondrocytes were treated with T-2 toxin(1~20 ng/ml)for 5 d.Fas,p53 and other apoptosis-related proteins such as Bax,Bcl-2,Bcl-xL,caspase-3 were determined by Western blot analysis and their mRNA expressions were determined by reverse transcriptase-polymerase chain reaction(RT-PCR).Results:Increases in Fas,p53 and the pro-apoptotic factor Bax protein and mRNA expressions and a decrease of the anti-apoptotic factor Bcl-xL were observed in a dose-dependent manner after exposures to 1~20 ng/ml T-2 toxin,while the expression of the anti-apoptotic factor Bcl-2 was unchanged.Meanwhile,T-2 toxin could also up-regulate the expressions of both pro-caspase-3 and caspase-3 in a dose-dependent manner.Conclusion:These data suggest a possible underlying molecular mechanism for T-2 toxin to induce the apoptosis sig- naling pathway in human chondrocytes by regulation of apoptosis-related proteins. 关 键 词:毒素 细胞凋亡 软骨细胞 化学分析
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