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我们以往的研究工作证实了硫化氢(hydrogen sulfide,H2S)对甲醛神经毒性和氧化应激具有拮抗作用.Paraoxonase-1(PON-1)是机体重要的内源性抗氧化剂.本研究的目的是探讨PON-1是否可介导H2S的抗甲醛神经毒性作用.采用甲醛损伤PC12细胞为甲醛神经毒性的细胞模型.硫氢化钠(NaHS,一种H2S的供体)不仅可以上调PC12细胞PON-1的活力,还可恢复甲醛对PC12细胞PON-1表达与活力的抑制作用.2-hydroxyquinoline(2-HQ)是一种选择性PON-1抑制剂,它可显著降低H2S对甲醛细胞毒性、凋亡和活性氧(reactive oxygen species,ROS)累积的抑制作用.而且,2-HQ可阻止H2S逆转甲醛激活PC12细胞caspase-3和下调PC12细胞bcl-2表达.结果提示H2S依赖PON-1去保护PC12细胞对抗甲醛的神经毒性.我们的这一发现表明PON-1有希望成为防治甲醛神经损伤的新靶点.
Our previous studies confirmed that hydrogen sulfide (H2S) antagonizes formaldehyde neurotoxicity and oxidative stress.Paraoxonase-1 (PON-1) is an important endogenous antioxidant in the body.Our goal is To explore whether PON-1 can mediate the anti-formaldehyde neurotoxicity of H2S.Formaldehyde-induced cellular model of PC12 cells injured by formaldehyde is used.Hydrogen sodium sulfide (a donor of H2S) can not only upregulate PON-1 2-hydroxyquinoline (2-HQ) is a selective inhibitor of PON-1, which can significantly reduce the toxicity of H2S to formaldehyde cells, and the inhibitory effects of formaldehyde on PON-1 expression in PC12 cells. 2-HQ can prevent H 2 S from reversing formaldehyde and activating caspase-3 in PC12 cells and down-regulating the expression of bcl-2 in PC12 cells, suggesting that H2S is dependent on PON-1 for deprotection The Neurotoxicity of PC12 Cells Against Formaldehyde Our finding suggests that PON-1 is promising as a new target for the prevention of formaldehyde-induced nerve damage.