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中文摘要：
目的研究T-2毒素对软骨细胞P53、Bcl-xL和Caspase-3表达的影响以及硒对T-2毒素致软骨细胞损伤的保护作用。方法胎儿软骨细胞体外培养5d，向培养液中加入硒（100μg/L）和不同浓度的T-2毒素（1、10、20μg／L），采用Western blot分析软骨细胞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-3 mRNA的表达。结果各T-2毒素组与对照组比较，不同浓度的T-2毒素（1-20μg／L）均能引起P53蛋白表达水平明显升高和Bcl-xL蛋白表达水平下降（P〈0.05）；当T-2毒素浓度达10-20μg/L时，Caspase-3蛋白和mRNA表达水平均升高（P〈0．05）；当T-2毒素浓度达20μg/L时，P53的mRNA表达水平明显升高（P〈0．05）。各T-2毒素组与T-2毒素加硒组比较，硒可部分对抗T-2毒素引起的P53表达的升高和Bcl-xL表达的下降，同时，降低Caspase-3表达水平（P〈0．05）。结论T-2毒素诱导的凋亡与其上调软骨细胞P53、Caspase-3表达，同时下调Bcl-xL表达水平有关；硒可部分对抗P53、Caspase-3和Bcl-xL表达的变化，对软骨细胞有保护作用。
英文摘要：
Objective To determine the effect of T-2 toxin and selenium on the protein expression of P53, Bcl-xL and Caspase-3 in chondrocytes,and to known the molecular targets and mechanisms of T-2 toxin induced apoptosis,the protective effects of selenium in the T-2 toxin induced apoptosis. Methods The human chondrocytes were treated with T-2 toxin （1-20 μg/L） and selenium （100μg/L） for 5 days. The protein expression of 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 antiapoptotic factor Bcl-xL were observed in a dose-dependent manner after exposure of 1-20μg/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 easpase-3 in a dose-dependent manner. Selenium down regulated P53 and Caspase-3 expression and up regulated Bcl-xL expression induced by T-2 toxin. Conclusion These data suggest a possible underlying molecular mechanism whereby T-2 toxin could induce the apoptosis signaling pathway in human chondrocytes by the regulation of apoptosis-related proteins P53,Bcl-xL and Caspase-3. Selenium has a protective effect by partly blocking the increased expression of P53 and Caspase-3, as well as decreased expression of Bcl-xL induced by T-2 toxin.
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