烟酰胺核糖对MPP+诱导SH-SY5Y细胞损伤的保护及机制研究

Protective effects and mechanisms of nicotinamide riboside on MPP+-induced injury in SH-SY5Y cells

摘要:

目的 探究烟酰胺核糖（NR）对1-甲基-4-苯基-吡啶离子（MPP⁺）诱导的SH-SY5Y细胞损伤的保护作用及其潜在机制。方法 取对数生长期的H-SY5Y细胞来完成实验，使用3 mmol/L MPP⁺处理细胞构建帕金森病（PD）体外模型。细胞分为对照组（常规培养）、MPP⁺组（MPP⁺处理）、实验组（0.5 mmol/L NR和MPP⁺处理）。细胞培养后检测细胞存活率、凋亡率，氧化应激水平［活性氧（ROS）、丙二醛（MDA）、超氧化物歧化酶（SOD）］，炎症水平［白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）］，烟酰胺腺嘌呤二核苷酸（NAD⁺）水平等指标。结果 与对照组比较，MPP⁺组细胞凋亡率、ROS、MDA、TNF-α、IL-6水平均升高（P <0.05），细胞存活率、SOD、NAD⁺水平均降低（P <0.05）；与MPP⁺组比较，实验组细胞凋亡率、ROS、MDA、TNF-α、IL-6水平均降低（P <0.05），细胞存活率、SOD、NAD⁺水平均升高（P <0.05）。结论 NR可以减轻MPP⁺诱导的神经细胞损伤，其机制可能与补充NAD⁺减轻细胞氧化应激和炎症反应有关。

Abstract:

Objective To explore the protective effect and mechanism of nicotinamide riboside (NR) on SH-SY5Y cells damage induced by MPP⁺.Methods SH-SY5Y cells in the logarithmic growth stage were used in the experiment. Cells were treated with 3 mmol/L MPP⁺ to establish Parkinson disease (PD) model. The cells were divided into control group (cells were cultured normally), MPP⁺ group(cells treated with MPP⁺)，NR group(cells treated with MPP⁺ and 0.5 mmol/L NR).After culturing, cell survival rate, apoptosis rate, oxidative stress level [reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD)], inflammation level[interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α)] and nicotinamide adenine dinucleotide (NAD⁺) levels were detected.Results Compared with the control group, the cell apoptosis, ROS, MDA content, TNF-α, and IL-6 were increased, while the cell survival rate, SOD activity and NAD⁺ levels were decreased (P <0.05) in the MPP⁺ group. Compared with the MPP⁺ group, the ROS, MDA content, TNF-α, and IL-6 levels were significantly decreased, while the cell survival rate, SOD activity and NAD⁺ levels were significantly increased (P <0.05) in the NR group.Conclusion NR attenuates MPP⁺-induced injury in neural cells, which may be involved in oxidative stress and inflammation through NAD⁺ supplementation.