摘要
目的观察帕金森病(PD)模型大鼠纹状体内的氧化应激指标及细胞凋亡相关蛋白的表达。方法大鼠右侧纹状体内注入6-羟基多巴胺(6-OHDA)制备帕金森病模型,4周后观察行为学改变,5周后检测正常对照、假手术和模型组大鼠纹状体内超氧化物歧化酶(SOD)、谷胱苷肽过氧化物酶(GSH-Px)活性、还原型谷胱甘肽(GSH)及丙二醛(MDA)含量变化,Western方法检测Bax和Bcl-2蛋白表达。结果在成功筛选的10只帕金森病模型大鼠右侧纹状体中,与自身对侧、正常对照及假手术组同侧相比,其SOD、GSH-Px活性,GSH含量均下降,而MDA含量升高(均P<0.05);与正常对照及假手术组同侧相比,其Bax蛋白表达增高,而Bcl-2蛋白表达下降。结论氧化应激在帕金森病发病机制中起到重要作用,而Bax和Bcl-2蛋白参与了氧化应激诱导细胞凋亡的调控过程。
Objective To study the oxidative stress and apoptosis relative protein expression in rat striatum during the pathogenesis of Parkinson＇s disease （PD） induced by 6-hydroxydopamine （6-OHDA）. Methods 6-OHDA was stereotacticly injected into the right striatum of the rats at two sites to produce PD models. Activities of superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, contents of reduced glutathione （GSH） and malondialdehyde （MDA） in the injured and normal striatum were measured using assay kits; and levels of Bax and Bcl-2 were detected by Western blotting in injured striatum. Results In 10 successful PD rats, compared with either the sham group or the normal group, activities of SOD and GSH-Px and contents of GSH in the right striatum significantly decreased while contents of MDA increased obviously （P〈0.05）; And levels of Bax significantly increased while expression of Bel-2 obviously decreased. Conclusion Oxidative stress plays a key role in the pathogenesis of PD. Furthermore, Bax and Bel-2 were involved in the regulation of apoptosis under oxidative stress induced by 6-OHDA.
出处
《中国康复理论与实践》
CSCD
2009年第5期431-433,共3页
Chinese Journal of Rehabilitation Theory and Practice
基金
国家863基金项目(2006AA02A408)
