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目的:建立3种帕金森病小鼠模型,观察牵正散提取物对小鼠行为学影响,初步探讨其作用机制。方法:1昆明小鼠随机分组,设立模型组,牵正散低、高剂量组(1.7,5.0 g·kg-1),阳性药组(盐酸苯海索,3.35 mg·kg-1)。各治疗组小鼠连续ig给药4 d。末次给药后1 h,各组ip给予氢溴酸槟榔碱(25 mg·kg-1)或氧化震颤素(0.15 mg·kg-1)。记录各组小鼠震颤潜伏期和震颤持续时间。2C57BL/6小鼠随机分组,设立正常组,模型组,牵正散低、高剂量组剂量组(1.7,5.0 g·kg-1),阳性药组(美多芭,50 mg·kg-1)。除正常组,各组小鼠ip给予1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP,30 mg·kg-1),连续5 d。第6天开始治疗组ig给予牵正散提取物和美多芭,连续7 d,末次给药后检测小鼠行为学变化,电镜观察黑质神经元结构变化。结果:1小鼠ip槟榔碱或氧化震颤素后出现明显震颤,与模型组比较,牵正散提取物高剂量组震颤潜伏期显著延长(P<0.05),低、高剂量组震颤持续时间均显著缩短(P<0.01)。2与模型组比较,小鼠ip MPTP后出现明显运动障碍,黑质神经元超微结构明显损伤,经牵正散提取物处理后,小鼠自主活动次数增加、转棒潜伏期延长、爬杆时间缩短(P<0.05),黑质神经元线粒体等结构损伤程度减轻。结论:牵正散提取物显著抑制帕金森病模型小鼠震颤、改善运动障碍,其作用机制可能与减轻线粒体损伤、保护神经元有关。
OBJECTIVE: To establish three mouse models of Parkinson’s disease and observe the behavioral effects of Qianzhao powder extract on mice and to explore its mechanism. Kunming mice were randomly divided into two groups: model group, Qianzhengsan low and high dose group (1.7, 5.0 g · kg -1), positive group (trihexyphenidyl hydrochloride, 3.35 mg · kg -1). Mice in each treatment group were administered ig for 4 consecutive days. At 1 h after the last administration, arecoline hydrobromide (25 mg · kg-1) or oxotrelin (0.15 mg · kg-1) were given ip in each group. The latency of the tremor and the duration of tremor in the mice in each group were recorded. The 2C57BL / 6 mice were randomly divided into three groups: normal group, model group, Qianzao powder group, high dose group (1.7, 5.0 g · kg -1), positive group ). In addition to the normal group, mice in each group were given 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg · kg-1) ip for 5 days. On the 6th day, the rats in the treatment group were given igazhuosan extract and metoprolol for 7 consecutive days. The behavioral changes of the mice were detected after the last administration, and the changes of the structure of the substantia nigra neurons were observed by electron microscope. Results: Compared with the model group, the latency of tremor in the high-dose Qianzhao powder group was significantly prolonged (P <0.05), and the duration of tremor in the low-dose and high-dose groups was significant Shortened (P <0.01). 2 Compared with the model group, obvious dyskinesia appeared after MPTP in mice, and the ultrastructure of substantia nigra neurons was obviously damaged. After treated by Qianzheng powder, the number of spontaneous activity in mice increased, the latency of rotarod prolonged, (P <0.05), mitochondria and other structural damage in substantia nigra neurons reduced. Conclusion: The extract of Qianzheng San significantly inhibits the rat model of Parkinson’s disease, tremor and improve dyskinesia, the mechanism may be mitochondrial mitochondrial damage and protect neurons.