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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。方法收集本院2013年7月~2015年7月病例,将存在蛋白酶体功能障碍的帕金森病患者50例作为观察组,未存在蛋白酶体功能障碍的帕金森病患者50例作为对照组,观察2组患者的行为学改变情况,通过RT-PCR、Western blotting分子生物学方法检测患者血液中α-突触核蛋白(α-Syn)表达水平。结果观察组患者血清的α-突触核蛋白表达水平显著高于对照组(P<0.05)。结论蛋白酶体功能障碍可能导致散发性帕金森病患者血液中α-突触核蛋白(α-Syn)水平升高,考虑该因素可能是散发性帕金森疾病的危险因素。
Objective To investigate the pathogenesis of sporadic Parkinson’s disease caused by proteasome dysfunction. Methods From July 2013 to July 2015 in our hospital, 50 patients with Parkinson’s disease who had proteasome dysfunction were selected as the observation group and 50 patients with Parkinson’s disease without proteasome dysfunction as the control group. Two groups of patients with behavioral changes, by RT-PCR, Western blotting molecular biology methods to detect the level of α-synuclein (α-Syn) in patients with blood. Results The level of α-synuclein expression in observation group was significantly higher than that in control group (P <0.05). Conclusions Proteasome dysfunction may lead to elevated α-syn level in the blood of patients with sporadic Parkinson’s disease. Considering this factor may be a risk factor for sporadic Parkinson’s disease.