期刊
NEUROSCIENCE
卷 448, 期 -, 页码 94-106出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2020.09.027
关键词
ischemic stroke; urolithin A; apoptosis; neuroinflammation; neurogenesis
资金
- National Natural Science Foundation of China [81371217]
- Research Grant of Guangdong Province Key Laboratory of Psychiatric Disorders [N201901]
- Innovation and Strong College Program of Guangdong [2018KTSCX183]
- Natural Science Foundation of Guangdong [2017A030313520, 2017A030313899]
- Science and Technology Foundation of Guangdong Province [2016A020214019]
- Science and Technology Foundation of Guangzhou [201707010231]
- Science Foundation of Education Bureau of Guangzhou City [1201610239]
Neuroinflammation contributes to neuronal death in cerebral ischemia. Urolithin A (UA), a gut microbial metabolite of ellagic acid, has emerged as a potential anti-inflammatory agent. However, its roles and precise mechanisms in stroke remain unknown. Here we found that UA treatment ameliorated infarction, neurological deficit scores, and spatial memory deficits after cerebral ischemia. Furthermore, UA significantly reduced neuron loss and promoted neurogenesis after ischemic stroke. We also found that UA attenuated apoptosis by regulating apoptotic-related proteins. Meanwhile, UA treatment inhibited glial activation via affecting inflammatory signaling pathways, specifically by enhancing cerebral AMPK and I kappa Ba activation while decreasing the activation of Akt, P65NF kappa B, ERK, JNK, and P38MAPK. Our findings reveal a key role of UA against ischemic stroke through modulating apoptosis and neuroinflammation in mice. (C) 2020 IBRO. Published by Elsevier Ltd. All rights reserved.
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