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作 者:朱美娥[1] 舒丹[2] 陈江帆[3] 何金彩[1]
机构地区:[1]温州医学院附属一院脑科中心,浙江温州325000 [2]温州医学院心理学系,浙江温州325000 [3]美国波士顿大学医学院神经科分子神经药理实验室,美国波士顿200020
出 处:《中风与神经疾病杂志》2009年第3期333-335,共3页Journal of Apoplexy and Nervous Diseases
摘 要:目的探讨川芎嗪对MPTP所致小鼠多巴胺能神经元损伤的保护作用及可能机制。方法C57BL/6J雄性小鼠32只,随机分为4组:生理盐水对照组(NS+NS)、生理盐水组(NS+MPTP)、川芎嗪高剂量组(LT50+MPTP)、川芎嗪低剂量组(LT20+MPTP),每组8只动物。分别采用HPLC法检测纹状体中DA的含量,免疫组化检测黑质中TH阳性细胞数,荧光显色法检测黑质SOD活力、GSH含量。结果LT50+MPTP组纹状体DA含量、黑质DA神经元数量、黑质SOD活力、黑质GSH含量较NS+MPTP组显著增高(P<0.01)。结论川芎嗪对对MPTP所致的小鼠多巴胺能神经元损伤具有保护作用,其保护机制可能与其调节调节小鼠黑质中的SOD、GSH含量有关。Objective To investigate the neuroproteetive effects and mechanisms of ligustrazine on the MPTP-indueed dopaminergic neurodegeneration in a mouse model of PD. Methods Male C57BL/6J mice were randomly divided into following four treatment groups ( n = 8/group) : ( 1 ) the saline control group ( NS + NS), mice pretreated with saline followed by saline treatment;(2) the mide pre-treated with saline followed by saline treatment (NS + MPTP) ; (3) the mice pretreated with 50mg/kg of ligustrazine followed by MPTP treatment ( LT50 + MPTP) ; (4) the mice pretreated with 20mg/kg of ligustrazine followed by MPTP (LT20 + MPTP). HPLC, immunohistoehemistry and fluorimetry were used. Resuits The residual DA eontents ,TH-IR positive cells, SOD activity and GSH content in the mice pretreated with 50mg/kg ligustrazine ( LT50 + MPTP) were significantly higher than those of the saline-pretreatd mice ( NS + MPTP) ( P 〈 0.01 ). Conclusions Ligustrazine ameliorated MPTP-induced dopaminergic neurodegeneration in mice. The neuroprotective effect of ligustrazine may be associated with their strong antioxidant eapaeity in vivo.
关 键 词:C57BL/6J雄性小鼠 PD MPTP 川芎嗪 抗氧化作用
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