Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, Medical College of Qingdao University, Qingdao 266071, China.
Neuropharmacology. 2011 Jul-Aug;61(1-2):329-35. doi: 10.1016/j.neuropharm.2011.04.021. Epub 2011 Apr 23.
Increasing evidence suggests that oxidative stress may be implicated in the degeneration of dopaminergic neurons in Parkinson's disease (PD), and anti-oxidation have been shown to be effective to PD treatment. Myricetin has been reported to have the biological functions of anti-oxidation, anti-apoptosis, anti-inflammation and iron-chelation. The aim of the present study is to investigate the neuroprotective effect of myricetin on 1-methyl-4-phenylpyridinium (MPP(+))-treated MES23.5 cells and the underlying mechanisms. The results showed that myricetin treatment significantly attenuated MPP(+)-induced cell loss and nuclear condensation. Further experiments demonstrated that myricetin could suppress the production of intracellular reactive oxygen species (ROS), restore the mitochondrial transmembrane potential (▵Ψm), increase Bcl-2/Bax ratio and decrease caspase-3 activation that induced by MPP(+). Futhermore, we also showed myricetin decreased the phosphorylation of mitogen-activated protein kinase (MAPK) kinase 4 (MKK4) and c-Jun N-terminal kinase (JNK) caused by MPP(+). These results suggest that myricetin protected the MPP(+)-treated MES23.5 cells by anti-oxidation and inhibition of MKK4 and JNK activation.
越来越多的证据表明，氧化应激可能与帕金森病（PD）中多巴胺能神经元的退化有关，抗氧化作用已被证明对 PD 的治疗有效。杨梅素具有抗氧化、抗凋亡、抗炎和铁螯合等生物学功能。本研究旨在探讨杨梅素对 1-甲基-4-苯基吡啶（MPP(+))处理的 MES23.5 细胞的神经保护作用及其机制。结果表明，杨梅素处理可显著减轻 MPP(+）诱导的细胞死亡和核固缩。进一步的实验表明，杨梅素可以抑制 MPP(+）诱导的细胞内活性氧（ROS）的产生，恢复线粒体跨膜电位（▵Ψm），增加 Bcl-2/Bax 比值，降低 caspase-3 的激活。此外，我们还发现杨梅素降低了 MPP(+）引起的丝裂原活化蛋白激酶（MAPK）激酶 4（MKK4）和 c-Jun N 端激酶（JNK）的磷酸化。这些结果表明，杨梅素通过抗氧化和抑制 MKK4 和 JNK 的激活来保护 MPP(+）处理的 MES23.5 细胞。
