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目的:通过研究拜颤停复方(BCT)对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)致小鼠帕金森病(PD)模型神经行为学、纹状体多巴胺(DA)含量、氧化应激反应的影响,探讨BCT对PD模型神经保护作用的可能作用机制。方法:雄性C57BL/6小鼠,MPTP-HC1(30 mg·kg-1·d-1,ip,0.9%生理盐水溶解)5 d,造成PD小鼠模型;设立正常组、模型组、多巴丝肼组(62.50 mg·kg-1·d-1)及BCT高、中、低剂量组(363.00,181.50,95.75 mg·kg-1·d-1),各给药组均用0.5%羧甲基纤维素钠(CMC-Na)溶解;BCT高、中、低剂量组ig给药治疗20 d后,进行爬杆实验和自主活动实验以观察小鼠行为学的变化;采用UPLC-MS-MS三重四级杆串联质谱技术检测小鼠纹状体多巴胺(DA)的含量;化学比色法检测小鼠黑质(SN)部位超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)及单胺氧化酶B(MAO-B)。结果:与正常组比较,模型组小鼠爬杆时间显著延长(P<0.05),自主活动次数显著减少(P<0.05),纹状体DA含量、SOD及GSH-Px水平显著降低(P<0.01),MDA及MAO-B水平显著升高(P<0.01)。与模型组比较,经过BCT治疗,PD小鼠的神经行为学得到显著改善(P<0.05),纹状体DA含量,SOD及GSH-Px水平显著升高(P<0.01,P<0.05),MDA及MAO-B水平显著降低(P<0.01)。结论:BCT可以通过提高机体的抗氧化和清除自由基能力,明显改善PD小鼠的神经行为学变化及纹状体DA的含量,是其对PD模型神经保护作用的可能机制。
OBJECTIVE: To investigate the neurobehavioral, neuroprotective and antihypertensive effect of Parkinson’s disease (PD) induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) Striatal dopamine (DA) content, oxidative stress response to explore the possible role of BCT on the PD model of neuroprotective effect mechanism. Methods: Male C57BL / 6 mice were induced with MPTP-HC1 (30 mg · kg-1 · d-1, ip, 0.9% (62.50 mg · kg-1 · d-1) and BCT high, medium and low dose groups (363.00,181.50,95.75 mg · kg-1 · d-1) MSCs were dissolved in CMC-Na, and BCG high, medium and low dose groups were treated with ig for 20 days, and then the pole-climbing experiment and autonomic activity test were performed to observe the changes of mice behavior. MS was used to detect the content of dopamine (DA) in mouse striatum. The contents of superoxide dismutase (SOD), malondialdehyde (MDA) Glutathione peroxidase (GSH-Px) and monoamine oxidase B (MAO-B). Results: Compared with the normal group, the climbing time of mice in the model group was significantly longer (P <0.05), the number of spontaneous activity was significantly decreased (P <0.05), DA content in the striatum, SOD and GSH-Px were significantly decreased 0.01), MDA and MAO-B levels were significantly increased (P <0.01). Compared with the model group, the neurobehavioral changes of PD mice were significantly improved (P <0.05), the contents of DA, the levels of SOD and GSH-Px in striatum were significantly increased (P <0.01, P <0.05) MDA and MAO-B levels decreased significantly (P <0.01). CONCLUSION: BCT can significantly improve the neurobehavioral changes and the content of DA in striatum in PD mice by increasing the antioxidant and scavenging ability of free radicals, which is a possible mechanism of neuroprotection on PD model.