引用本文:卢健军,王展航,王玉周,潘梦秋,匡祖颖,叶锦龙,李 波,徐 炎.蛋白酶体功能障碍对散发性帕金森病发病机制影响的探讨[J].中国临床新医学,2017,10(12):1176-1179.
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蛋白酶体功能障碍对散发性帕金森病发病机制影响的探讨
卢健军,王展航,王玉周,潘梦秋,匡祖颖,叶锦龙,李 波,徐 炎
510510 广州,广东三九脑科医院神经内一科
摘要:
[摘要] 目的 探讨蛋白酶体功能障碍对散发性帕金森病的发病机制的影响。方法 观察组大鼠50只,将蛋白酶抑制剂注入大鼠的右侧黑质致密部位,构建蛋白酶体功能障碍模型,对照组大鼠50只采用生理盐水注射。观察两组大鼠的行为学改变情况,通过HE染色检测路易(小)体形成率,半定量逆转录聚合酶链反应(RT-PCR)、Western blotting分子生物学方法检测黑质部位α-突触核蛋白(α-Syn)表达情况。结果 观察组路易(小)体形成率高于对照组(P<0.01)。RT-PCR、Western blotting分子生物学检测结果显示观察组α-Syn显著高于对照组(P<0.01)。结论 蛋白酶体功能障碍可以导致路易(小)体形成率及黑质部位α-Syn形成,是散发性帕金森病的危险因素。
关键词:  路易(小)体形成率  α-突触核蛋白  散发性帕金森  发病机制
DOI:10.3969/j.issn.1674-3806.2017.12.14
分类号:R 741
基金项目:
Effect of proteasome dysfunction on the pathogenesis of sporadic Parkinson′s disease
LU Jian-jun, WANG Zhan-hang, WANG Yu-zhou, et al.
The First Department of Neurology, Guangdong 999 Brain Hospital, Guangzhou 510510, China
Abstract:
[Abstract] Objective To investigate the effect of proteasome dysfunction on the pathogenesis of sporadic Parkinson′s disease.Methods The rat model of proteasome dysfunction was made by injecting protease inhibitor into the right site of substantia nigra(the observation group, n=50). The rats in the control group(n=50) were injected with saline injection(n=50). The changes of behavior, the Louis(small) formation rate evaluated by HE staining and the expression of α-synuclein(α-Syn) in substantia nigra detected by reverse transcription-polymerase chain reaction(RT-PCR) and Western blotting molecular biology were compared between the two groups.Results The Louis(small) formation rate in the observation group was significantly higher than that in the control group(P<0.01). The levels of the expression of α-Syn in the observation group were significantly higher than those in the control group(P<0.01).Conclusion Proteasome dysfunction can lead to high Louis(small) formation rate and the expression of α-Syn in the substantia nigra, which is a risk factor for the pathogenesis of sporadic Parkinson′s disease.
Key words:  Louis(small) formation rate  α- synuclein(α-Syn)  Sporadic Parkinson  Pathogenesis