Ghrelin prevents 1-methyl-4-phenylpyridinium ion-induced cytotoxicity through antioxidation and NF-kappaB modulation in MES23.5 cells.

Abstract:

:Ghrelin, a 28-amino acid peptide, is an endogenous ligand for the growth hormone secretagogue (GHS) receptor. Our previous data showed that ghrelin could inhibit apoptosis in Parkinson's disease (PD) models both in vitro and in vivo. There is now growing evidence that oxidative stress has a critical role in the etiology of PD. And ghrelin was reported to possess anti-inflammatory, antioxidant effects. Dose ghrelin protect dopaminergic neurons by its antioxidant effect? In the present study, 1-methyl-4-phenylpyridinium (MPP(+)) was used to evaluate the possible antioxidant effects of ghrelin on MPP(+)-induced neurotoxicity in MES23.5 cells and the underlying mechanisms. Our results showed that MPP(+) significantly increased malonaldehyde (MDA) level and Bax/Bcl2 ratio, reduced the level of Cu-Zn superoxide dismutase (SOD) and catalase (CAT). Ghrelin protected MES23.5 cells against MPP(+)-induced neurotoxicity by reversing these changes. Furthermore, ghrelin pretreatment significantly inhibited MPP(+)-induced nuclear factor-kappaB translocation. These results suggest that the protective effects of ghrelin on MPP(+)-induced cytotoxicity may be ascribed to its antioxidative properties, and the modulation of nuclear factor-kappaB.

journal_name

Exp Neurol

journal_title

Experimental neurology

authors

Liu L,Xu H,Jiang H,Wang J,Song N,Xie J

doi

10.1016/j.expneurol.2009.11.009

subject

Has Abstract

pub_date

2010-03-01 00:00:00

pages

25-9

issue

1

eissn

0014-4886

issn

1090-2430

pii

S0014-4886(09)00467-1

journal_volume

222

pub_type

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