Protective effects of β- nicotinamide adenine dinucleotide against motor deficits and dopaminergic neuronal damage in a mouse model of Parkinson's disease
Protective effects of β- nicotinamide adenine dinucleotide against motor deficits and dopaminergic neuronal damage in a mouse model of Parkinson's disease
复制标题
β-烟酰胺腺嘌呤二核苷酸对帕金森病小鼠模型运动缺陷和多巴胺能神经元损伤的保护作用
DOI：
10.1016/j.pnpbp.2019.109670
复制
发表时间：
2019
影响因子：
5.6
通讯作者：
Jian-min Liu
中科院分区：
文献类型：
--
作者：
Chang Shan;Yan-ling Gong;Qian-qian Zhuang;Yan-fang Hou;Shu-min Wang;Qin Zhu;Guo-rui Huang;Bei Tao;Li-hao Sun;Hong-yan Zhao;Sheng-tian Li;Jian-min Liu
The level of nicotinamide adenine dinucleotide (NAD) decreases in Parkinson's disease (PD), and its reduction has been reported to be involved in many age-associated neurodegenerative pathologies. Thus, we investigated whether NAD replenishment is beneficial in a 6-hydroxydopamine (6-OHDA)-induced mouse model of PD. Preinjection with NAD in the striatum ameliorated motor deficits and dopaminergic neuronal damage in the substantia nigra and striatum of a mouse model of PD. Moreover, preincubation with NAD protected PC12 cells against the loss of cell viability, morphological damage, oxidative stress and mitochondrial dysfunction caused by 6-OHDA. These results add credence to the beneficial role of NAD against parkinsonian neurodegeneration in mouse models of PD, provide evidence for the potential of NAD for the prevention of PD, and suggest that NAD prevents pathological changes in PD via decreasing mitochondrial dysfunctions.
