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Neuroprotective effects of α‐melanocyte‐stimulating hormone against the neurotoxicity of 1‐methyl‐4‐phenylpyridinium
Author(s) -
Peng Tao,
Wang Jingtao,
Lu Jingjing,
Lu Hong,
Teng Junfang,
Jia Yanjie
Publication year - 2017
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.1385
Subject(s) - neuroprotection , oxidative stress , neurotoxicity , cytochrome c , medicine , apoptosis , reactive oxygen species , chemistry , endocrinology , viability assay , lactate dehydrogenase , programmed cell death , mitochondrion , melanocyte stimulating hormone , pharmacology , hormone , biology , biochemistry , toxicity , enzyme
Parkinson's disease (PD) is the second most common neurodegenerative disease in humans. The hormone α‐melanocyte‐stimulating hormone (α‐MSH) has been reported to be neuroprotective in previous studies. The aim of this study is to investigate the neuroprotective effects of α‐MSH against the neurotoxicity of 1‐methyl‐4‐phenylpyridinium (MPP+). Our results indicated that treatment with α‐MSH in M17 cells attenuated MPP+‐induced oxidative stress, embodied by exacerbated reactive oxygen species and protein carbonyls. In addition, we found that α‐MSH could improve mitochondrial function in M17 cells through increasing the level of adenosine triphosphate and mitochondrial membrane potential. Furthermore, treatment with α‐MSH restored the reduction of cell viability and the induction of lactate dehydrogenase release induced by α‐MSH. Importantly, Hoechst staining results indicated that α‐MSH treatment significantly reduces the number of apoptotic cells after treatment with MPP+. Mechanically, we found that α‐MSH prevented apoptosis signals through reducing the level of cleaved caspase‐3 and attenuating cytochrome c release. All these data imply that α‐MSH produces a protective effect in PD. © 2015 IUBMB Life, 69(5):315–320, 2017