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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Differential effect of platelet activating factor on 1-methyl-4-phenylpyridinium-induced cell death through regulation of apoptosis-related protein activation.
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Differential effect of platelet activating factor on 1-methyl-4-phenylpyridinium-induced cell death through regulation of apoptosis-related protein activation.

机译：血小板活化因子通过调节细胞凋亡相关蛋白的活化对1-甲基-4-苯基吡啶鎓诱导的细胞死亡的差异作用。

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摘要

Platelet activating factor (PAF) has been suggested to play a critical role in the pathogenesis of neurological disorders. We assessed the effect of PAF against the toxicity of 1-methyl-4-phenylpyridinium (MPP(+)), a parkinsonian toxin, in relation to apoptotic process. PAF exhibited differential effect against the MPP(+) toxicity in differentiated PC12 cells depending on concentration. Treatment with 0.75 microM PAF significantly attenuated the MPP(+)-induced increase in Bax levels, decrease in Bid and Bcl-2 levels, and mitochondrial membrane potential loss that lead to the release of cytochrome c and subsequent caspase-3 activation. The inhibitory effect of PAF was not associated with nuclear factor-kappaB activation. In contrast, PAF at the concentrations greater than 2.5 microM exhibited a toxicity and additive effect on the MPP(+) toxicity. The results show that PAF at low concentrations, which does not induce a significant toxicity, may prevent the MPP(+) toxicity by suppressing the apoptosis-related protein activation and mitochondrial membrane permeability change that lead to the cytochrome c release and caspase-3 activation. The preventive effect seems to be associated with the inhibitory effect on the formation of reactive oxygen species and depletion of GSH. In contrast, PAF at higher concentrations may exhibit an additive toxic effect against the MPP(+) toxicity by increasing apoptosis-related protein activation.
机译：已经建议血小板活化因子（PAF）在神经系统疾病的发病机理中起关键作用。我们评估了PAF对帕金森氏毒素1-甲基-4-苯基吡啶鎓（MPP（+））的凋亡过程的影响。 PAF在浓度不同的PC12细胞中对MPP（+）毒性表现出不同的作用。 0.75 microM PAF的治疗显着减弱了MPP（+）诱导的Bax水平升高，Bid和Bcl-2水平降低以及线粒体膜电位丧失，从而导致细胞色素c释放和随后的caspase-3活化。 PAF的抑制作用与核因子-κB激活无关。相反，浓度大于2.5 microM的PAF表现出对MPP（+）毒性的毒性和加性效应。结果表明，低浓度的PAF不会引起明显的毒性，它可以通过抑制凋亡相关的蛋白激活和线粒体膜通透性变化（导致细胞色素c释放和caspase-3激活）来预防MPP（+）毒性。 。预防作用似乎与对活性氧的形成和谷胱甘肽耗竭的抑制作用有关。相比之下，较高浓度的PAF可能通过增加凋亡相关的蛋白激活而表现出对MPP（+）毒性的加成毒性作用。

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