Nicotinamide mononucleotide improves energy activity and survival rate in an in vitro model of Parkinson’s disease

作者：Lei Lü, Le Tang, Wenshi Wei, Yunyi Hong, Heyu Chen, Weihai Ying, Shengdi Chen · 发表于：Experimental and Therapeutic Medicine · 年份：2014 · DOI：10.3892/etm.2014.1842 · 被引用次数：60 · 研究领域：PARP inhibition in cancer therapy、Autophagy in Disease and Therapy、Calcium signaling and nucleotide metabolism

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 cell...