FSD-C10抑制MPTP诱导的帕金森病小鼠氧化应激及炎性反应研究

Study on FSD-C10 Inhibiting Oxidative and Inflammatory Responses in MPTP Induced Parkinson's Disease Mice

关键词:  帕金森病  FSD-C10  氧化应激  抗炎作用

Key words:  Parkinson's disease  FSD-C10  oxidative stress  anti-inflammatory effect

摘要:

目的 研究口服FSD-C10对帕金森病（Parkinson's disease，PD）小鼠的治疗作用，并探讨其相关机制。方法 小鼠随机分为正常组、PD组和FSD-C10组（50 mg·kg^-1），旷场行为学测试评估小鼠移动的总距离、休息时间、穿格次数；Western blotting检测脑组织酪氨酸羟化酶（tyrosine hydroxylase，TH）、ROCKⅡ；比色法检测脑组织过氧化氢酶（catalase，CAT）、还原型谷胱甘肽（glutathione，GSH）、丙二醛和一氧化氮（nitric oxide，NO）；ELISA检测脑组织肿瘤坏死因子（tumor necrosis factor-α，TNF-α）、白介素-1β（interleukin-1β，IL-1β）及白介素-6（interleukin-6，IL-6）。结果 与正常组比较，PD组小鼠移动的总距离、穿格次数降低（P<0.01），休息时间延长（P<0.01），TH表达降低（P<0.05），ROCKⅡ表达增高（P<0.05），CAT活力下降（P<0.05），GSH含量降低（P<0.01），丙二醛含量升高（P<0.05），TNF-α、IL-1β、IL-6及NO升高（P<0.05或P<0.01）。与PD组比较，FSD-C10组小鼠移动的总距离、穿格次数增加（P<0.05），休息时间缩短（P<0.01），TH表达增高（P<0.05），ROCKⅡ表达降低（P<0.05），CAT活力增加（P<0.01），GSH含量升高（P<0.01），丙二醛含量降低（P<0.01），TNF-α、IL-1β、IL-6及NO下降（P<0.01）。结论 口服FSD-C10可以改善PD小鼠的行为学表现，对PD有明确的治疗作用，其作用机制可能与恢复氧化-抗氧化体系平衡、减少炎性因子分泌相关。

Abstract:

OBJECTIVE To explore the therapeutic effect and related mechanism of oral administration of FSD-C10 on Parkinson's disease(PD) mice. METHODS Mice were randomly divided into normal group, PD group and FSD-C10 group (50 mg·kg^-1). The total distance, rest time and crossing numbers were evaluated by open field test. Tyrosine hydroxylase(TH) and ROCKⅡ in the brain were detected by Western blotting. Catalase(CAT), glutathione(GSH), malondialdehyde and nitric oxide(NO) were detected by colorimetric method. The levels of inflammatory factors tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β) and interleukin-6(IL-6) in the brain were measured by ELISA. RESULTS Compared with the normal group, the total distance and the crossing numbers were decreased(P<0.01), the rest time was increased(P<0.01), the level of TH was decreased(P<0.05), the level of ROCKⅡ was increased(P<0.05), the activity of CAT was decreased(P<0.05), the concentration of GSH was decreased(P<0.01), the concentration of malondialdehyde was increased (P<0.05), and the concentrations of inflammatory factors TNF-α, IL-1β, IL-6 and NO were increased(P<0.05 or P<0.01) in the PD group. Compared with the PD group, the total distance and the crossing numbers were increased(P<0.05), the rest time was decreased(P<0.01), the level of TH was increased(P<0.05), the level of ROCKⅡ was decreased(P<0.05), the activity of CAT was increased(P<0.01), the concentration of GSH was increased(P<0.01), the concentration of malondialdehyde was decreased (P<0.01), and the concentrations of inflammatory factors TNF-α, IL-1β, IL-6 and NO were decreased(P<0.01) in the FSD-C10 group. CONCLUSION Oral administration of FSD-C10 can improve the behavior of PD mice, and has a clear therapeutic effect in PD mice. The therapeutic effect may be related to the recovery of the balance of oxidation-antioxidation system and the reduction of the secretion of inflammatory factors.