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目的 探讨T 2毒素对软骨细胞凋亡的作用,和对凋亡调控蛋白Bcl 2 与Bax表达的影响,以及微量元素硒对软骨细胞的保护作用。方法 采用电镜,Annexin V/PI法检测T 2 毒素致人软骨细胞凋亡的情况,采用流式细胞仪检测凋亡相关蛋白Bcl 2和Bax的表达。结果 T 2 毒素可引起软骨细胞发生凋亡的典型电镜形态改变;不同浓度(1~20μg/L)的T 2毒素均可以引起软骨细胞早期凋亡率和晚期凋亡率明显增加,且在一定范围内呈浓度依赖性,T 2毒素浓度为20μg/L时早期凋亡率最高达5.60%,晚期凋亡率最高达8.61%。生理浓度的微量元素硒可部分减弱T 2毒素引起的凋亡;不同浓度(1~20μg/L)的T 2毒素都能引起Bcl 2和Bax表达水平提高,浓度为10~20μg/L时,Bax/Bcl 2比值升高;硒能部分对抗T 2 毒素引起的Bcl 2 和Bax 表达的提高,使Bax/Bcl 2 比值下降,以降低凋亡率。结论 T 2毒素在浓度为1 ~ 20μg/L 时,可以引起软骨细胞凋亡; T 2 毒素引起的软骨细胞凋亡与软骨细胞内Bax/Bcl 2比值升高有关,硒对T 2毒素引起的软骨细胞凋亡有一定保护作用。
Objective To investigate the effect of T 2 toxin on chondrocyte apoptosis and its effect on the expression of Bcl 2 and Bax, as well as the protective effect of trace element selenium on chondrocytes. Methods The apoptosis of human chondrocytes induced by T 2 toxin was detected by electron microscopy and Annexin V / PI. The expressions of Bcl-2 and Bax were detected by flow cytometry. Results T 2 toxin could induce morphological changes of chondrocytes apoptosis. T 2 toxin with different concentration (1 ~ 20μg / L) could induce the early apoptosis rate and late apoptosis rate of chondrocytes significantly increased, The concentration of T 2 toxin was 20μg / L, the highest apoptosis rate was 5.60% and the late apoptosis rate was up to 8.61%. Physiological concentration of trace element selenium partially attenuated T 2 toxin-induced apoptosis; T 2 toxin at different concentrations (1 ~ 20 μg / L) could induce the expression of Bcl 2 and Bax at 10 ~ 20 μg / L, Bax / Bcl2 ratio increased; selenium partially against T 2 toxin-induced increase of Bcl 2 and Bax, Bax / Bcl 2 ratio decreased to reduce the rate of apoptosis. Conclusions T 2 toxin can cause chondrocyte apoptosis at the concentration of 1 ~ 20 μg / L; T 2 toxin-induced chondrocyte apoptosis is related to the increase of Bax / Bcl 2 ratio in chondrocytes; Chondrocyte apoptosis has a certain protective effect.