期刊
NEURAL REGENERATION RESEARCH
卷 10, 期 9, 页码 1433-1440出版社
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/1673-5374.165511
关键词
nerve regeneration; brain Injury; oxygen-glucose deprivation; cerebral ischemia; stroke; autophagy; beta-site APP-cleaving enzyme 1 (BACE1); beta-amyloid peptide; 3-methyladenine (3-MA); Rapamycin; neural regeneration
资金
- National Natural Science Foundation of China [31171014, 31371065]
- Shanghai Municipal Health Bureau, China [20134125]
- Shanghai Pudong District Health Bureau of China [PDZz2013-10]
Our previous findings have demonstrated that autophagy regulation can alleviate the decline of learning and memory by eliminating deposition of extracellular beta-amyloid peptide (A beta) in the brain after stroke, but the exact mechanism is unclear. It is presumed that the regulation of beta-site APP-cleaving enzyme 1 (BACE1), the rate-limiting enzyme in metabolism of A beta, would be a key site. Neuro-2a/amyloid precursor protein 695 (APP695) cell models of cerebral ischemia were established by oxygen-glucose deprivation to investigate the effects of Rapamycin (an autophagy inducer) or 3-methyladenine (an autophagy inhibitor) on the expression of BACE1. Either oxygen-glucose deprivation or Rapamycin down-regulated the expression of BACE1 while 3-methyladenine up-regulated BACE1 expression. These results confirm that oxygen-glucose deprivation down-regulates BACE1 expression in Neuro-2a/APP695 cells through the introduction of autophagy.
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