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Myricetin attenuated MPP(+)-induced cytotoxicity by anti-oxidation and inhibition of MKK4 and JNK activation in MES23.5 cells.

Abstract：

: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.

journal_name

Neuropharmacology

journal_title

Neuropharmacology

authors

Zhang K,Ma Z,Wang J,Xie A,Xie J

doi

10.1016/j.neuropharm.2011.04.021

subject

Has Abstract

pub_date

2011-07-01 00:00:00

pages

329-35

issue

1-2

eissn

0028-3908

issn

1873-7064

pii

S0028-3908(11)00166-3

journal_volume

61

pub_type

杂志文章

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