论文部分内容阅读
目的:探讨PC12细胞缺氧/再给氧损伤的信号转导机理。方法:培养的PC12细胞先缺氧(95％N2/5％CO2)6h,然后重新给氧,观测不同时间点细胞的存活率和caspase-3的活性;用MTT法测存活率,caspase-3检测试剂盒测caspase-3活性。用p38拮抗剂SB203580孵育细胞2h,之后缺氧/再给氧,观察SB203580对细胞存活率和caspase-3活性的影响。结果:PC12细胞缺氧/再给氧后caspase-3活性明显增加并使细胞存活率下降,SB203580明显降低缺氧/复氧后caspase-3的活性并使细胞死亡减少。结论:PC12细胞缺氧/再给氧后至少可以通过激活p38、caspase-3信号分子诱导PC12细胞死亡。
Objective: To investigate the signal transduction mechanism of hypoxic / reoxygenation injury in PC12 cells. Methods: The cultured PC12 cells were hypoxic (95% N2 / 5% CO2) for 6 hours and then reoxygenated to observe the cell viability and caspase-3 activity at different time points. The survival rate, caspase-3 Test kit measured caspase-3 activity. The cells were incubated with p38 antagonist SB203580 for 2 hours, followed by hypoxia / reoxygenation. The effects of SB203580 on cell viability and caspase-3 activity were observed. Results: After hypoxia / reoxygenation, the activity of caspase-3 in PC12 cells was significantly increased and the cell viability was decreased. SB203580 significantly reduced the activity of caspase-3 after hypoxia / reoxygenation and decreased cell death. CONCLUSION: PC12 cells can induce PC12 cell death by activating p38 and caspase-3 signaling molecules after anoxia / reoxygenation.