神经退行性变
安普克
小檗碱
蛋白激酶A
PI3K/AKT/mTOR通路
蛋白激酶B
神经炎症
雷帕霉素的作用靶点
兴奋毒性
自噬
医学
激活剂(遗传学)
AMP活化蛋白激酶
生物
神经保护
谷氨酸受体
细胞生物学
药理学
激酶
生物化学
信号转导
炎症
细胞凋亡
内科学
免疫学
受体
疾病
基因
作者
Siru Qin,Huiling Tang,Wei Li,Yinan Gong,Shanshan Li,Jin Huang,Yuxin Fang,Wenjuan Yuan,Yangyang Liu,Shenjun Wang,Yongming Guo,Yi Guo,Zhifang Xu
标识
DOI:10.2174/1381612826666200523172334
摘要
Neurodegenerative disorders are heterogeneous diseases associated with either acute or progressive neurodegeneration, causing the loss of neurons and axons in the central nervous system (CNS), showing high morbidity and mortality, and there are only a few effective therapies. Here, we summarized that the energy sensor adenosine 5‘-monophosphate (AMP)-activated protein kinase (AMPK), and its agonist berberine can combat the common underlying pathological events of neurodegeneration, including oxidative stress, neuroinflammation, mitochondrial disorder, glutamate excitotoxicity, apoptosis, autophagy disorder, and disruption of neurovascular units. The abovementioned effects of berberine may primarily depend on activating AMPK and its downstream targets, such as the mammalian target of rapamycin (mTOR), sirtuin1 (SIRT1), nuclear factor erythroid-2 related factor-2 (Nrf2), nuclear factor-κB (NF-κB), phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), nicotinamide adenine dinucleotide (NAD+), and p38 mitogen-activated protein kinase (p38 MAPK). It is hoped that this review will provide a strong basis for further scientific exploration and development of berberine's therapeutic potential against neurodegeneration.
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