丙泊酚通过p38丝裂原活化蛋白激酶依赖性途径减轻氧化应激诱导的PC12细胞损伤。
Propofol attenuates oxidative stress-induced PC12 cell injury via p38 MAP kinase dependent pathway.
作者信息
Wu Xing-jun, Zheng Yong-jun, Cui Yong-yao, Zhu Liang, Lu Yang, Chen Hong-zhuan
机构信息
Department of Pharmacy, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
出版信息
Acta Pharmacol Sin. 2007 Aug;28(8):1123-8. doi: 10.1111/j.1745-7254.2007.00610.x.
AIM
To investigate the neuroprotective effect of propofol and its intracellular mechanism on neurons in vitro.
METHODS
Cell viability was determined with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide reduction. Apoptotic cell death was determined by Hoechst 33258 staining and a fluorescence-activated cell sorter. The caspase-3 activity was measured by fluorometric assay. Mitogen-activated protein (MAP) kinase phosphorylation was detected with Western blotting.
RESULTS
The pretreatment of rat pheochromocytoma cell line PC12 with propofol (1-10 micromol/L) resulted in a significant recovery from hydrogen peroxide (H2O2)-induced cell death and the inhibition of H2O2 induced caspase-3 activation and PC12 cell apoptosis. Propofol inhibited the H2O2-induced p38 MAP kinase, but not c-Jun N-terminal kinase or extracellular signal-regulated kinase 1 and 2 activations.
CONCLUSION
Propofol might attenuate H2O2-induced PC12 cell death through the inhibition of signaling pathways mediated by the p38 MAP kinase.
目的
研究丙泊酚对体外培养神经元的神经保护作用及其细胞内机制。
方法
采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐还原法测定细胞活力。通过Hoechst 33258染色和荧光激活细胞分选仪检测凋亡细胞死亡情况。采用荧光分析法测定半胱天冬酶-3活性。用蛋白质印迹法检测丝裂原活化蛋白(MAP)激酶磷酸化情况。
结果
用丙泊酚(1-10微摩尔/升)预处理大鼠嗜铬细胞瘤细胞系PC12，可使其从过氧化氢(H2O2)诱导的细胞死亡中显著恢复，并抑制H2O2诱导的半胱天冬酶-3活化和PC12细胞凋亡。丙泊酚抑制H2O2诱导的p38 MAP激酶活化，但不抑制c-Jun氨基末端激酶或细胞外信号调节激酶1和2的活化。
结论
丙泊酚可能通过抑制p38 MAP激酶介导的信号通路减轻H2O2诱导的PC12细胞死亡。
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