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中文摘要：
目的观察T-2毒素对软骨细胞P53、Bcl—xL和Caspase-3表达的影响。方法采用胎儿软骨细胞体外培养，培养基中加入不同浓度的T-2毒素（1～20μg／L）连续培养5d。采用Westernblot检测软骨细胞P53、Bcl—xL和Caspase-3蛋白表达水平；用RT—PCR法检测软骨细胞P53、Bcl—xL和Caspase-3mRNA的表达。结果与对照组比较，不同浓度（1—20μg/L）的T-2毒素均能引起Caspase-3蛋白表达水平升高而Bcl—xL蛋白表达水平下降（P〈0．05）；当T-2毒素浓度达到10-20μg/L时，P53蛋白和Caspase-3mRNA表达水平明显升高（P〈0．05）而Bcl—xLmRNA的表达水平无显著性下调（P〉0．05）；T-2毒素浓度达到20μg／L可以引起P53mRNA表达水平明显升高（P〈0．05）。结论T-2毒素诱导软骨细胞发生的凋亡可能与T-2毒素上调软骨细胞P53、Caspase-3表达，同时下调Bcl—xL表达有关。
英文摘要：
Objective To determine the effect of T- 2 toxin on P53, Bcl -xL and Caspase -3 expression in chondrocytes, in order to know molecular targets and mechanisms of T - 2 toxin induced apoptosis. Methods The fetal chondrocytes were treated with T - 2 toxin （ 1 - 20 μg/L） for 5 days. P53, Bcl - xL and Caspase - 3 were determined by Western blot analysis and their mRNA expression were determined by RT - PCR. Results An increase in P53 and a decrease in expression of the anti - apoptotic factor Bcl - xL were observed in a dose - dependent manner after exposure of 10 - 20 μg/L T - 2 toxin, while the expression of the Bcl - xL mRNA was unchanged. Meanwhile, T - 2 toxin could also up - regulate the expression of both pro - caspase - 3 and caspase - 3 in a dose - dependent manner. Conclusions These data suggest a possible underlying molecular mechanism whereby T - 2 toxin could induce the apoptosis signaling pathway in fetal chondrocytes by the regulation of apoptosis - related proteins P53, Bcl -xL and Caspase -3.
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