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目的研究过氧化物酶体增生物激活受体γ共激活因子1-α(PGC-1α)对铅致小鼠睾丸支持(TM4)细胞毒性的拮抗作用。方法将处于对数生长期的TM4细胞和慢病毒干扰技术构建稳定的PGC-1α过表达小鼠睾丸支持[PGC-1α(+)TM4]细胞株分别暴露于0(对照)、20、40、80、160μmol/L乙酸铅溶液染毒24 h。采用流式细胞仪检测细胞凋亡率,并测定细胞内Caspase-9、Caspase-3的活力。结果与对照组比较,各浓度乙酸铅染毒组TM4细胞和PGC-1α(+)TM4细胞的凋亡率均升高,差异均有统计学意义(P<0.05);且随着乙酸铅浓度升高,TM4细胞和PGC-1α(+)TM4细胞的凋亡率均呈上升趋势。与相同浓度TM4细胞比较,各浓度乙酸铅染毒组PGC-1α(+)TM4细胞的凋亡率较低,差异均有统计学意义(P<0.05)。与对照组比较,各浓度乙酸铅染毒组TM4细胞和PGC-1α(+)TM4细胞内Caspase-9和Caspase-3的活力均升高,除20μmol/L乙酸铅染毒组TM4细胞内Caspase-3活力外,差异均有统计学意义(P<0.05);且随着乙酸铅染毒浓度的升高,TM4细胞和PGC-1α(+)TM4细胞内Caspase-9和Caspase-3的活力均呈上升趋势。与相同浓度TM4细胞比较,各浓度乙酸铅染毒组PGC-1α(+)TM4细胞内Caspase-9和Caspase-3的活力较低,差异均有统计学意义(P<0.05)。结论PGC-1α可能通过下调细胞内凋亡相关蛋白Caspase-9、Caspase-3的活力,来拮抗铅诱导的小鼠睾丸支持细胞凋亡。
Objective To investigate the antagonism of peroxisome proliferator-activated receptor γ-coactivator 1-α (PGC-1α) on cytotoxicity of lead-induced mouse testis support (TM4). Methods TMT cells in PGT-1α (+) TM4] cell lines with stable PGC-1α overexpression were exposed to 0 (control), 20, 40, 80,160μmol / L lead acetate solution for 24 h. The apoptosis rate was detected by flow cytometry, and the activity of Caspase-9 and Caspase-3 in cells was determined. Results Compared with the control group, the apoptotic rates of TM4 cells and PGC-1α (+) TM4 cells treated with lead acetate at various concentrations were significantly increased (P <0.05). With the increase of lead acetate concentration The apoptosis rate of TM4 cells and PGC-1α (+) TM4 cells all showed an upward trend. Compared with the same concentration of TM4 cells, the apoptotic rate of PGC-1α (+) TM4 cells treated with lead acetate at different concentrations was lower, with statistical significance (P <0.05). Compared with the control group, the activities of Caspase-9 and Caspase-3 in TM4 cells and PGC-1α (+) TM4 cells treated with lead acetate at different concentrations were higher than those in the control group. Except for 20μmol / L lead acetate-treated cells, (P <0.05). With the increase of the concentration of lead acetate, the activities of Caspase-9 and Caspase-3 in TM4 cells and PGC-1α (+) TM4 cells were significantly increased All showed an upward trend. Compared with the same concentration of TM4 cells, the activities of Caspase-9 and Caspase-3 in PGC-1α (+) TM4 cells were lower than those in the control group (P <0.05). Conclusion PGC-1α may antagonize the lead-induced apoptosis of testicular sertoli cells in mice by down-regulating the activity of apoptosis-related proteins Caspase-9 and Caspase-3.