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Nicotinamide Mononucleotide Can Decrease Rotenone‐Induced Necrosis and Apoptotic Changes of Neuro2a Cells
Author(s) -
Tang Le,
Chen Shengdi,
Ying Weihai
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.763.8
Subject(s) - nicotinamide mononucleotide , rotenone , apoptosis , nad+ kinase , necrosis , programmed cell death , viability assay , nicotinamide , chemistry , mitochondrion , nicotinamide phosphoribosyltransferase , biochemistry , microbiology and biotechnology , pharmacology , biology , nicotinamide adenine dinucleotide , enzyme , genetics
Our laboratory has found that NAD+ can profoundly decrease cell necrosis induced by genotoxic agents, and NAD+ administration can significantly reduce ischemic brain damage. In this study we tested our hypothesis that nicotinamide mononucleotide (NMN)‐‐‐ the precursor of NAD+ ‐‐‐ may also decrease mitochondtial inhibitor‐induced cell death. Our study using LDH assay showed that 0.5 micromolar rotenone induced approximately 40% decreases in the survival of Neuro2a cells, which was significantly attenuated by treatment of 0.1 to 10 mM NMN. Our study applying MTT assay further indicated that 0.1 to 10 mM NMN can attenuate rotenone‐induced decreases in cell viability. We also found that NMN treatment can attenuate the rotenone‐induced nuclear condensation ‐‐‐ a hallmark of apoptosis ‐‐‐ of the cells. Collectively, our study has indicated that NMN can attenue both the rotenine‐induced necrosis and apoptotic changes of Neuro2a cells, suggesting that NMN may be used to decrease mitochondrial inhibition‐induced cell death in neurological diseases (Supported by a Key Research Grant of Shanghai Municipal Scientific Committee 08JC1415400 (WY), Pujiang Scholar Program Grant (WY), and Shanghai Med‐X Engineering Center Grant of Equipment and Technology of Physical Therapy for Major Diseases (WY)).