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作 者:吴静[1] 易香华[1] 侯秋科[1] 邓汝东[1] 李伊为[1] 周健洪[1] 伍艺灵[1] 陈东风[1]
机构地区:[1]广州中医药大学解剖学教研室,广州510006
出 处:《解剖学杂志》2009年第5期647-650,共4页Chinese Journal of Anatomy
基 金:国家自然科学基金(30472272,30772861)
摘 要:目的:进一步探讨神经生长因子(NGF)/酪氨酸受体激酶A(TrkA)通路是否为龟板抗帕金森病(PD)大鼠多巴胺能神经元凋亡中的机制。方法:采用大鼠左侧黑质致密带注射6-羟基多巴胺(6-OHDA,0.2%)μl造成PD模型,同时设立龟板组、模型组和正常对照组,用免疫组织化学显色方法观察PD大鼠中脑黑质NGF、TrkA和磷酸化的糖原合成酶激酶-3p(p-GSK-3p)阳性神经元数目。免疫印迹法检测NGF、TrkA、p-GSK-3β蛋白表达水平的变化。结果:免疫组织化学显色显示龟板组PD大鼠中脑黑质致密部NGF、TrkA的阳性细胞数明显多于模型组。免疫印迹法结果显示龟板组PD大鼠中脑黑质致密部NGF、TrkA的蛋白表达水平高于模型组。结论:龟板能上调6-OHDA诱导的PD大鼠中脑黑质NGF、TrkA和p-GSK-3β的表达,这可能是其抗PD大鼠多巴胺能神经元凋亡的分子机制。Objective: To explore whether NGF/TrkA pathway participates in antiapoptotic effect of plastrum testudinis (PT) on neurons of substantia nigra of Parkinson's disease (PD) rat induced by 6-hydroxydopamine (6-OHDA). Methods: Rat PD model was induced by injection of 6-OHDA (0. 2μ, 2μl into the left compact zone of the substantia nigra. Rats were randomly divided into model control, normal control and PT treatment groups, which was administrated intragastrical- ly of 2g PT twice daily for 12 weeks. The number of NGF, TrkA and p-GSK-3β positive cells in substantia nigra was meas- ured with SABC immunohistochemical method, and the expression of NGF, TrkA and p-GSK-3β was detected by Western blot. Results: The number of NGF, TrkA and p-GSK-3β positive cells in substantia nigra was significantly increased in the PT treatment group compared with that in the model control group. The expression of NGF, TrkA and p-GSK-3β was also enhanced in the PT treatment group. Conclusion: PT can promote the expression of NGF, TrkA and pGSK-3β in the substantia nigra of PD rats induced by 6-OHDA, which may involve in its antiapoptotic effect in dopaminergic neurons of PD.
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