碱性成纤维细胞生长因子对PC12细胞氧化损伤的保护作用和机制

Protective Effect and Mechanism of Basic Fibroblast Growth Factor on PC12 Cells Injury

探讨碱性成纤维细胞生长因子(bFGF)对H2O2诱导PC12细胞凋亡的影响及其作用机制。利用H2O2诱导的PC12细胞建立细胞氧化损伤模型,用不同浓度的bFGF进行药物干预,CCK-8法和流式细胞技术检测细胞存活率和凋亡率,试剂盒测定超氧化物歧化酶(SOD)活性,Western blot检测ERK1/2和p-ERK1/2蛋白表达。bFGF处理的PC12细胞存活率较对照组高;H2O2处理的PC12细胞SOD活性降低,bFGF+H2O2组SOD活性显著升高;bFGF预处理细胞2h后细胞凋亡率下降;在加入MEK1/2的特异性阻断剂U0126 10μmol/L预处理细胞后,再先后分别用bFGF和H2O2刺激细胞,PC12细胞p-ERK1/2蛋白水平显著降低(P<0.01)。结果表明bFGF可以通过抗氧化和抑制细胞凋亡作用,来对抗H2O2对PC12细胞的氧化损伤作用,其机制与MEK-ERK信号途径有关。

The effects and the mechanism of basic fibroblast growth factor（bFGF） on H2O2 induced apoptosis in PC12 cells were investigated.The model of cellular oxidation damage was established by H2O2 induced PC12 cells,and the cell livability and apoptosis rate were detection by CCK-8 and cytometry with different concentration of bFGF to medical interventions,then superoxide dismutase（SOD） activity was measured by SOD kit,and ERK1/2 andp-ERK1/2,expression were analyzed by Western blot.The viability of PC12 cells increased after treated with bFGF compared with control group.SOD activities of PC12 cells after treated H2O2 group were lower,however,whichwere higher in bFGF＋H2O2 group than that in H2O2 group.After bFGF was pretreatment for 2h,the apoptotic rates decreased.After the cells were pretreated adding MEK1/2 specific inhibitor p-ERK1/2,then that were stimulated by bFGF and H2O2,respectively,and the level of p-ERK1/2,decreased significantly（P0 01）.The bFGF can restrain apoptosis of oxidation injury PC12 cells with H2O2 by oxidation resistance and inhibition apoptosis,and the mechanism was involved with signal pathway of MEK-ERK.