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作 者:刘人恺[1] 冯莉[1] 肖波[1] 罗晨[1] 吴志国[1] 龙莉莉[1] 卢晓琴[1]
出 处:《临床神经病学杂志》2009年第2期116-119,共4页Journal of Clinical Neurology
基 金:国家自然科学基金(30770736)
摘 要:目的探讨幽门螺杆菌(HP)对多巴胺能细胞系SH-SY5Y的损伤作用及其机制。方法体外培养多巴胺能细胞系SH-SY5Y细胞分别加入HP上清蛋白(HP组)、1-甲基-4-苯基-吡啶离子(MPP+)(PD组)和培养液(对照组),用噻唑蓝(MTT)染色法检测细胞存活率,用共聚焦显微镜、分光光度仪检测细胞内活性氧(ROS)和线粒体呼吸链酶复合体活性。结果HP组和PD组细胞的存活率明显下降,高浓度HP组细胞生存率明显低于中、低浓度HP组(均P<0.05)。与对照组比较,HP组和PD组细胞内ROS水平明显减少、线粒体呼吸链酶复合体活性下降(均P<0.05)。结论HP分泌成分对多巴胺能细胞有与MPP+相似的损伤作用,氧化应激反应及线粒体功能受损可能是其导致多巴胺能细胞损伤的机制。Objective To study the damage effects and its mechanism of Helicobacter pylori (HP) on dopaminergie cell line SH-SYSY in vitro. Methods The cellular survival rate, the level of cellular activated oxygen and the activity of mitochondrion respiratory chain complexes were measured in dopaminergic cell line SH-SYSY after adding secretory components of HP( HP group), MPP^+ (PD group) and culture solution( control group). Results The cellular survival rates in the HP group and PD group were decreased, the cellular survival rate of high concentration HP subgroup was dramatically decreased than those in the middle and low concentration subgroups( all P 〈 0. 05). Comparing with the control group, the level of cellular activated oxygen, the activity of mitochondrion respiratory chain complexes in the HP group and PD group were decreased obviously( all P 〈 0. 05 ). Conclusion The mechanism of dopaminergie cells injury induced by secretory components of HP as MPP ^+ may be oxidative stress and the damage of function of mitochondrion.
分 类 号:R742.5[医药卫生—神经病学与精神病学]
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