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In Vitro Protective Effects Of Pyrroloquinoline Quinone On Methylmercury-induced Neurotoxicity

机译:吡咯并喹啉醌对甲基汞诱导的神经毒性的体外保护作用

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Methylmercury (MeHg), as a well-known neurotoxicant, has been implicated to induce massive neurode-generation. Pyrroloquinoline quinone (PQQ) is a novel redox cofactor and also exists in various plants and animal tissues. In vivo as well as in vitro experimental studies have shown that PQQ functions as an essential nutrient or antioxidant. In this study, we demonstrated the protective effects of PQQon MeHg-induced neurotoxicity in PC12 cells. The results showed that after pretreatment of PC12 cells with PQQ prior to MeHg exposure, the MeHg-induced cytotoxicity was significantly attenuated, and then DNA fragmentation was correspondingly reduced. PQQ prevented the disruption of mitochondrial membrane potential, up-regulated the level of Bcl-2, and consequently inhibited the activation of caspase-3. Moreover, PQQ also decreased the production of ROS and maintained the GSH levels in PC12 cells exposed to MeHg. Thus, these data indicate that PQQ can protect neurons against MeHg-induced apoptosis and oxidative stress via ameliorating the mitochondrial dysfunction. Data from this study provide a new useful strategy for the treatment of neuronal toxicity induced by mercury toxins.
机译:甲基汞(MeHg)作为一种众所周知的神经毒剂,被认为可诱导大量神经退行性病变。吡咯并喹啉醌(PQQ)是一种新型的氧化还原辅助因子,还存在于各种动植物组织中。体内和体外实验研究表明,PQQ作为必需的营养或抗氧化剂。在这项研究中,我们证明了PQQ对MeHg诱导的PC12细胞神经毒性的保护作用。结果表明,在暴露于MeHg之前,用PQQ预处理PC12细胞后,MeHg诱导的细胞毒性显着减弱,然后DNA断裂相应减少。 PQQ阻止了线粒体膜电位的破坏,上调了Bcl-2的水平,因此抑制了caspase-3的活化。此外,PQQ还降低了暴露于MeHg的PC12细胞中ROS的产生并维持了GSH的水平。因此,这些数据表明PQQ可通过减轻线粒体功能障碍来保护神经元免受MeHg诱导的细胞凋亡和氧化应激。这项研究的数据为治疗由汞毒素引起的神经元毒性提供了一种新的有用策略。

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