摘要
背景:氧化应激是包括阿尔茨海默氏病(AD)在内的多种疾病的主要特征。最近报道了氧固醇衍生物的参与。 目的:本研究的目的是评估氧化应激对AD患者胆固醇损伤的影响。 方法:对56例AD患者和97例对照进行了病例对照研究。用分光光度法对红细胞(RBC)和血浆进行了氧化生物标记物水平的测定,包括脂质过氧化产物和抗氧化酶活性。胆固醇前体和氧固醇(7-酮胆固醇(7KC),7α-羟基胆固醇(7α-OHC),7β-羟基胆固醇(7β-OHC),24S-羟基胆固醇(24S-OH),25-羟基胆固醇(25-OHC)和27-羟基胆固醇通过气相色谱-质谱法定量测定血浆中的(27-OHC)。 结果:在AD患者的RBC和血浆中,发现谷胱甘肽过氧化物酶(GPx)活性显着下降与丙二醛(MDA)水平升高相关。在AD患者中,与对照组相比,血浆AD患者血浆中的羊毛甾醇水平降低和7β-OHC,24S-OHC,27-OHC和25-OHC的积累也较高。小精神状态检查(MMSE)得分与血浆中的MDA和共轭二烯(CD)水平相关。此外,红细胞中的MDA水平与7β-OHC相关。二元逻辑回归显示GPx活性与AD之间存在关联(OR = 0.895,95%CI:0.848-0.945。P <0.001)。 结论:我们的数据巩固了AD中氧化还原稳态的破裂与脂质和胆固醇氧化之间的关系。
关键词: 阿尔茨海默氏病,氧化应激,氧固醇,脂质过氧化,抗氧化酶,胆固醇。
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