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Int. J. Mol. Sci. 2017, 18(5), 1012;

Atractylenolide-I Protects Human SH-SY5Y Cells from 1-Methyl-4-Phenylpyridinium-Induced Apoptotic Cell Death

Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Korea
Author to whom correspondence should be addressed.
Academic Editors: José L. Quiles and Maurizio Battino
Received: 24 January 2017 / Revised: 21 April 2017 / Accepted: 3 May 2017 / Published: 8 May 2017
(This article belongs to the Section Bioactives and Nutraceuticals)
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Oxidative stress and apoptosis are the major mechanisms that induce dopaminergic cell death. Our study investigates the protective effects of atractylenolide-I (ATR-I) on 1-methyl-4-phenylpyridinium (MPP+)-induced cytotoxicity in human dopaminergic SH-SY5Y cells, as well as its underlying mechanism. Our experimental data indicates that ATR-I significantly inhibits the loss of cell viability induced by MPP+ in SH-SY5Y cells. To further unravel the mechanism, we examined the effect of ATR-I on MPP+-induced apoptotic cell death characterized by an increase in the Bax/Bcl-2 mRNA ratio, the release of cytochrome-c, and the activation of caspase-3 leading to elevated levels of cleaved poly(ADP-ribose) polymerase (PARP) resulting in SH-SY5Y cell death. Our results demonstrated that ATR-I decreases the level of pro-apoptotic proteins induced by MPP+ and also restored Bax/Bcl-2 mRNA levels, which are critical for inducing apoptosis. In addition, ATR-I demonstrated a significant increase in the protein expression of heme-oxygenase in MPP+-treated SH-SY5Y cells. These results suggest that the pharmacological effect of ATR-I may be, at least in part, caused by the reduction in pro-apoptotic signals and also by induction of anti-oxidant protein. View Full-Text
Keywords: atractylenolide-I; apoptosis; MPP+; neuroprotection; Parkinson’s disease atractylenolide-I; apoptosis; MPP+; neuroprotection; Parkinson’s disease

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More, S.V.; Choi, D.-K. Atractylenolide-I Protects Human SH-SY5Y Cells from 1-Methyl-4-Phenylpyridinium-Induced Apoptotic Cell Death. Int. J. Mol. Sci. 2017, 18, 1012.

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