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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*

机译:T-2毒素诱导的人软骨细胞凋亡涉及Fas,p53,Bcl-xL,Bcl-2,Bax和caspase-3信号通路*

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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 signaling pathway in human chondrocytes by regulation of apoptosis-related proteins.
机译:目的:探讨T-2毒素对人软骨细胞Fas,p53,Bcl-xL,Bcl-2,Bax和caspase-3表达的影响。方法:用T-2毒素(1〜20 ng / ml)处理人软骨细胞5 d。通过蛋白质印迹分析确定Fas,p53和其他凋亡相关蛋白,例如Bax,Bcl-2,Bcl-xL,caspase-3,并通过逆转录聚合酶链反应(RT-PCR)确定其mRNA表达。结果:暴露于1〜20 ng / ml T-2后,Fas,p53和促凋亡因子Bax蛋白和mRNA表达增加,而抗凋亡因子Bcl-xL则呈剂量依赖性降低。毒素,而抗凋亡因子Bcl-2的表达未改变。同时,T-2毒素也可以剂量依赖性方式上调caspase-3和caspase-3的表达。结论:这些数据表明T-2毒素可能通过调控凋亡相关蛋白来诱导人软骨细胞凋亡信号通路的潜在分子机制。

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