Neuro-Behavioural Biology Center, Institute of Science and Technology for Research and Development, Mahidol University, Salaya, Nakhonpathom, Thailand.
J Pineal Res. 2009 Jan;46(1):36-42. doi: 10.1111/j.1600-079X.2008.00605.x. Epub 2008 May 27.
Neuroprotective effects of melatonin against oxidative stress-induced neuronal cell degeneration in human SH-SY5Y neuroblastoma cells were investigated in this report. The results demonstrate that exogenous administration of H(2)O(2) and 1-methyl, 4-phenyl, pyridinium ion (MPP(+)) significantly decreased cell viability in SH-SY5Y cultured cells. Desipramine, a monoamine uptake blocker was able to abolish the toxic effects of MPP(+) but not H(2)O(2) in reduction of cell viability. Conversely, melatonin reversed the toxic effects of H(2)O(2) and MPP(+) on cell viability. In addition, the reduction of phosphorylation of tyrosine hydroxylase, the rate limiting enzyme in dopamine synthesis, and phosphorylation of cyclic AMP responsive element-binding protein by H(2)O(2) and MPP(+) was also diminished by melatonin. These results demonstrate some effective roles of melatonin on neuroprotection and its action on the modulation of tyrosine hydroxylase phosphorylation.
本报告研究了褪黑素对人 SH-SY5Y 神经母细胞瘤细胞氧化应激诱导的神经元细胞变性的神经保护作用。结果表明，外源性 H2O2 和 1-甲基-4-苯基-吡啶鎓离子（MPP+）显著降低了 SH-SY5Y 培养细胞的活力。单胺摄取抑制剂去甲丙咪嗪能够消除 MPP+的毒性作用，但不能消除 H2O2 对细胞活力的降低作用。相反，褪黑素逆转了 H2O2 和 MPP+对细胞活力的毒性作用。此外，褪黑素还降低了 H2O2 和 MPP+对酪氨酸羟化酶磷酸化（多巴胺合成的限速酶）和环磷酸腺苷反应元件结合蛋白磷酸化的抑制作用。这些结果表明褪黑素在神经保护方面具有一定的作用，并且能够调节酪氨酸羟化酶的磷酸化。
