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Mitochonic acid 5 activates the MAPK–ERK–yap signaling pathways to protect mouse microglial BV-2 cells against TNFα-induced apoptosis via increased Bnip3-related mitophagy

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成果类型:
期刊论文
作者:
Lei, Qingyun;Tan, Jian;Yi, Shangqing;Wu, Na;Wang, Yilin;...
通讯作者:
Wu, Heng
作者机构:
[Yi, Shangqing; Wu, Heng; Wang, Yilin; Lei, Qingyun; Tan, Jian; Wu, Na] Univ South China, Hosp 1, Dept Neurol, Hengyang, Hunan, Peoples R China.
通讯机构:
[Wu, Heng] U
Univ South China, Hosp 1, Dept Neurol, Hengyang, Hunan, Peoples R China.
语种:
英文
关键词:
MA-5;Inflammatory injury;Mitophagy;Microglia;Mitochondria;MAPK–ERK–yap signaling pathway
期刊:
CELLULAR & MOLECULAR BIOLOGY LETTERS
ISSN:
1425-8153
年:
2018
卷:
23
期:
1
页码:
1-16
基金类别:
This study was supported by grants from the National Natural Science Foundation of China (Number: 801301495). The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.
机构署名:
本校为第一且通讯机构
院系归属:
医学院
摘要:
Background: The regulation of microglial function via mitochondrial homeostasis is important in the development of neuroinflammation. The underlying mechanism for this regulatory function remains unclear. In this study, we investigated the protective role of mitochonic acid 5 (MA-5) in microglial mitochondrial apoptosis following TNFα-induced inflammatory injury. Methods: TNFα was used to induce inflammatory injury in mouse microglial BV-2 cells with and without prior MA-5 treatment. Cellular apoptosis was assessed using the MTT and TUNEL ass...

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