中文摘要：

本研究的目的是探讨蝎毒耐热蛋白（SVHRP）对1-甲基4-苯基-1，2，3，6-四氢吡啶（MPTP）处理的伴有空间学习记忆障碍的Parkinson病（PD）小鼠的保护机制,实验共分4组：（1）正常对照组（NS＋NS），C57BL／6小鼠颈部皮下注射生理盐水（NS）连续8d，同时腹腔注射生理盐水，连续8d；（2）阴性对照组（NS＋SVHRP）：C57BL／6小鼠颈部皮下注射生理盐水，连续8d，同时腹腔注射SVHRP（0．01mg／kg）连续8d；（3）PD模型组（MPTP＋NS）：C57BL／6小鼠颈部皮下注射MPTP（20mg／kg）连续8d制备小鼠PD模型，腹腔注射生理盐水连续8d；（4）蝎毒治疗组（MPTP＋SVHRP）：C57BL／6小鼠颈部皮下注射MPTP（20mg/kg）连续8d，给药后腹腔注射SVHRP（0．01mg／kg）连续8d。行为学和形态学研究结果表明，正常对照组和阴性对照组的各项实验数据均无明显差别。爬竿和游泳实验结果表明，与正常对照组相比较，MPTP处理小鼠爬竿（P〈0．01）和游泳（P〈0．01）分数明显降低。Morris水迷宫实验中，MPTP处理小鼠寻找平台潜伏期明显延长（P〈0．01）；向目标游泳时间所占百分比明显降低（P〈0．01），而向对侧象限游泳时间所占百分比明显增加（P〈0．01）。免疫细胞化学染色结果表明，PD模型组小鼠中脑内黑质致密部呈酪氨酸羟化酶免疫反应阳性的神经元的数目较正常组明显减少（P〈0．01）；而海马内神经元型一氧化氮合酶（nNOS）免疫反应阳性的神经元数（P〈0．01）以及NO含量（P〈0．01）均较正常组明显增多。行为学结果表明，与PD组比较，SVHRP处理的PD小鼠的运动协调能力（P〈0．01）和空间学习记忆能力（P〈0．01）均具有明显改善。

英文摘要：

To explore the protective role and its underlying mechanisms of the scorpion venom heat resistent protein （SVHRP） on Parkinson＇s disease （PD） mice with spatial learning memory deficits indueed by 1-methyl-4-phenyl-1 ,2,3,6-tetrahydropyridine（MPTP）. The miee were divided into four groups, including normal saline （NS） ＋ NS group, NS ＋ SVHRP group, MPTP ＋ NS group and MPTP ＋ SVHRP group. NS and MPTP （20 mg/kg, s. e. ） were injected for8 days. SVHRP （0.01 mg/kg, i. p. ） was treated for 8 days. The behavioral results showed that the scores of MPTP-treated mice in the pole （ P 〈 0.01 ） and swim tests （ P 〈 0.01 ） were much lower than those of the control ones. In comparison of control mice, MPTP-treated mice showed signifieant longer latency （ P 〈0.01 ） to platform, less training quadrant （P 〈 0.01 ） and more opposite quadrant （P 〈 0.01 ） search time in Morris water maze. hnmunocytochemistry results showed large loss of TH-immunoreactive （IR） neurons in the substantia nigra compact （ P 〈 0.01 ） in MPTP-treated mice. Meanwhile, the number of nNOS-IR neurons （ P 〈 0.01 ） and the content of nitric oxide （ P 〈 0.01 ） in the hippocampus increased dramatically, compared with the control and therapy group. Furthermore, the therapy group reversed loss of tyrosine hydroxylase （ TH）-IR neurons in substantia nigra compact （ P 〈 0. 01 ）, locomotor harmony disability （ P 〈 0. 01 ） arid spatial learning memory deficits （ P 〈 0.01 ） compared with the model group. There was no difference i, nNOS-IR neurons and the content of nitric oxide in the hippocampus between the therapy and control groups. This study suggest that SVHRP exerted neuroprotection in MPTP-treated C57BL/6 mice via decreasing nNOS in the hippocampus.