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氧化应激对溶酶体储存与转运甲醛的影响
Effect of Oxidative Stress on Accommodation and Transportation of Formaldehyde by Lysosome
投稿时间:2017-02-16  修订日期:2017-04-12
中文关键词:  内源甲醛探针,溶酶体,双侧颈动脉不全结扎,氧化应激
英文关键词:endogenous formaldehyde probe, lysosome, bilateral carotid occlusion, oxidative stress
基金项目:国家重点基础研究发展计划(973)资助项目(2012CB911004)
作者单位E-mail
陈茜茜 中国科学院生物物理研究所脑与认知科学国家重点实验室北京 100101中国科学院大学北京 100049 chenxi1264@163.com 
苏 涛 中国科学院生物物理研究所脑与认知科学国家重点实验室北京 100101  
赫英舸 中国科学院生物物理研究所脑与认知科学国家重点实验室北京 100101  
赫荣乔 中国科学院生物物理研究所脑与认知科学国家重点实验室北京 100101 herq@ibp.ac.cn 
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中文摘要:
      内源甲醛代谢失调被认为是导致阿尔茨海默病的危险因素之一,甲醛蓄积会引起神经细胞的死亡和认知功能的降低.研究表明,细胞内甲醛分布于溶酶体内,而溶酶体功能异常与神经退行性疾病密切相关.本文采用甲醛特异荧光探针,在氧化应激条件下,检测到小鼠脑微血管内皮细胞株bEnd.3和小鼠神经瘤母细胞株N2a溶酶体内甲醛明显升高;在慢性脑低灌注大鼠动物模型中,其脑神经细胞的溶酶体内甲醛也升高(P < 0.01);LeuLeuOMe处理bEnd.3细胞,使其溶酶体膜通透性增加,导致细胞内甲醛蓄积,而胞外甲醛降低.以上结果证明,溶酶体具有储存和转运甲醛的功能,如果溶酶体出现结构与功能的异常,会导致甲醛代谢失调,造成认知损害.
英文摘要:
      Dysmetabolism of endogenous formaldehyde is regarded as one of the risk factors for the onset and progression of Alzheimer’s disease. Excess extracellular and intracellular formaldehyde induce neuron death, involving the impairment of cognitive ability. As previously reported, lysosome dysfunction plays an important role in neurodegenerative diseases and intracellular formaldehyde locates in the lysosome. Utilizing formaldehyde fluorescent probe, abnormally increase of the lysosomal formaldehyde was detected in the blood endothelial cell line (bEnd.3) and neuroblastoma N2a cells (N2a) from mouse brain under oxidative stress. Brain formaldehyde was significantly (P < 0.01) elevated in the chronic cerebral hypoperfusion rats compared with those with SHAM. LeuLeuOMe was used to induce the permeabilization of lysosome membrane in bEnd.3. After LeuLeuOMe tretment, higher intracellular and lower extracellular formaldehyde were measured by microplate reader and high performance liquid chromatography (HPLC) respectively. In other words, lysosome not only accommodates endogenous formaldehyde, but also transports the compound out of cells. Abnormal lysosome function causes dysmetabolism of formaldehyde, which is correlated with age-related cognitive impairment.
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