自噬
实验性自身免疫性脑脊髓炎
姜黄素
PI3K/AKT/mTOR通路
神经保护
蛋白激酶B
多发性硬化
中枢神经系统
信号转导
免疫系统
髓鞘
生物
癌症研究
免疫学
细胞生物学
医学
神经科学
药理学
细胞凋亡
生物化学
作者
Boyao Yuan,Sun Mengjiao,Cai-cai Bao,Li Xiaoling,Zhenxing Liu,Manxia Wang
标识
DOI:10.1016/j.jneuroim.2019.577067
摘要
Curcumin has been used in the study of central nervous system immune-related diseases and exerts a substantial neuroprotective effect. However, the mechanism remains unclear. The AKT/mTOR autophagy-related signalling pathway plays an important role in tumour therapy, but whether curcumin plays a therapeutic role in multiple sclerosis (MS) through this signalling pathway remains to be determined. As an animal model of MS, experimental autoimmune encephalomyelitis (EAE) is induced by the myelin glial glycoprotein MOG35-55 in female C57BL/6 mice. We first evaluated the changes in autophagy levels in EAE mice. Then, curcumin was intraperitoneally injected into the mice, and the expression of AKT/mTOR autophagy signalling pathway-related proteins was evaluated. Our data show that 1. autophagy defects can cause neuronal damage in EAE mice; and 2. curcumin may regulate the activation of autophagy in EAE mice by affecting the AKT/mTOR autophagy signalling pathway, further balancing central nervous system and peripheral autophagy.
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