title: Nicotinamide mononucleotide improves energy activity and survival rate in anin vitromodel of Parkinson's disease.
abstract: Nicotinamide adenine dinucleotide (NAD+) repletion has been shown to provide marked neuroprotection from genotoxic agent-induced neuronal and astrocyte cell death. One of the key precursors of NAD+is nicotinamide mononucleotide (NMN). Therefore, it was hypothesized that NMN may attenuate apoptosis and improve energy metabolism in Parkinson's disease (PD)-like behavioral and neuropathological changes, and produce significant beneficial effects. In this study, a cellular model of PD, using rotenone-treated PC12 cells, was established to test the hypothesis that NMN may decrease PD-like pathological changes. Experiments were carried out to investigate cell survival, including an intracellular lactate dehydrogenase (LDH) assay. Apoptotic and necrotic cell death, NAD+levels and ATP levels were also evaluated. It was observed that NMN was able to significantly attenuate the rotenone-induced reduction in the survival rate of PC12 cells, as assessed by MTT and LDH assays. NMN treatment also significantly reduced the rotenone-induced apoptosis of the cells, as assessed by flow cytometry-based Annexin V/7-aminoactinomycin D staining. Furthermore, NMN restored intracellular levels of NAD+and ATP in the rotenone-treated cells, thus demonstrating the capacity of NMN to ameliorate mitochondrial inhibitor-induced impairments of energy metabolism. The present study indicates that NMN produces significant beneficial effects by attenuating apoptosis and improving energy metabolism in a cellular model of PD. These results suggest that NMN may become a promising therapeutic drug for PD.
authors.affiliation: Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China ; School of Biomedical Engineering and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai 200030, P.R. China.
authors.forename: Lei
authors.initials: L
authors.lastname: Lu
authors.affiliation: Department of Neurology, Huadong Hospital, Fudan University, Shanghai 200040, P.R. China ; Department of Neurology and Institute of Neurology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, P.R. China.
authors.forename: LE
authors.initials: L
authors.lastname: Tang
authors.affiliation: Department of Neurology, Huadong Hospital, Fudan University, Shanghai 200040, P.R. China.
authors.forename: Wenshi
authors.initials: W
authors.lastname: Wei
authors.affiliation: School of Biomedical Engineering and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai 200030, P.R. China.
authors.forename: Yunyi
authors.initials: Y
authors.lastname: Hong
authors.affiliation: School of Biomedical Engineering and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai 200030, P.R. China.
authors.forename: Heyu
authors.initials: H
authors.lastname: Chen
authors.affiliation: School of Biomedical Engineering and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai 200030, P.R. China ; Department of Neurology and Institute of Neurology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, P.R. China.
authors.forename: Weihai
authors.initials: W
authors.lastname: Ying
authors.affiliation: Department of Neurology and Institute of Neurology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, P.R. China.
authors.forename: Shengdi
authors.initials: S
authors.lastname: Chen
keywords: Parkinson’s disease; cell survival; energy activity; nicotinamide mononucleotide