中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2015年
8期
1048-1052
,共5页
自噬%脑缺血损伤%信号转导通路%PI3K/Akt%AMPK%NF-κB%MAPK
自噬%腦缺血損傷%信號轉導通路%PI3K/Akt%AMPK%NF-κB%MAPK
자서%뇌결혈손상%신호전도통로%PI3K/Akt%AMPK%NF-κB%MAPK
autophagy%cerebral ischemic injury%signal trans-duction pathway%PI3K/Akt%AMPK%NF-κB%MAPK
自噬是一种细胞内成分自我降解的过程，包括自噬的诱导、自噬体膜的形成、自噬体的形成、自噬体与溶酶体的融合以及内容物的降解。自噬若适度激活，则促进细胞存活；若过度激活，则可加重细胞损伤，甚至导致细胞裂解和促进细胞死亡。该文主要从自噬的形成过程及分子机制、脑缺血后自噬的诱发因素、自噬参与脑缺血的信号转导通路及自噬在脑缺血损伤中的作用进行综述，为进一步研究自噬与脑缺血性损伤及其药物调控提供参考。
自噬是一種細胞內成分自我降解的過程，包括自噬的誘導、自噬體膜的形成、自噬體的形成、自噬體與溶酶體的融閤以及內容物的降解。自噬若適度激活，則促進細胞存活；若過度激活，則可加重細胞損傷，甚至導緻細胞裂解和促進細胞死亡。該文主要從自噬的形成過程及分子機製、腦缺血後自噬的誘髮因素、自噬參與腦缺血的信號轉導通路及自噬在腦缺血損傷中的作用進行綜述，為進一步研究自噬與腦缺血性損傷及其藥物調控提供參攷。
자서시일충세포내성분자아강해적과정，포괄자서적유도、자서체막적형성、자서체적형성、자서체여용매체적융합이급내용물적강해。자서약괄도격활，칙촉진세포존활；약과도격활，칙가가중세포손상，심지도치세포렬해화촉진세포사망。해문주요종자서적형성과정급분자궤제、뇌결혈후자서적유발인소、자서삼여뇌결혈적신호전도통로급자서재뇌결혈손상중적작용진행종술，위진일보연구자서여뇌결혈성손상급기약물조공제공삼고。
Autophagy, a process of intracellular component deg-radation, consists of initiation, vesicle membrane, vesicle ex-pansion and completion, vesicle fusion and autophagosome deg-radation. Moderate activation of autophagy may promote cell sur-vival, while excessive activation of autophagy may aggravate cell injury, or even lead to cell lysis and death. This paper mainly reviews the process and the molecular basis of autophagy, as well as trigger factors, signal transduction pathways involved in cere-bral ischemia, along with its effects on ischemic brain injury, which will provide a reference for further probe of autophagy in cerebral ischemic injury and its drug regulation.
