炎症体
ALDH2
启动(农业)
氧化应激
化学
上睑下垂
激活剂(遗传学)
生物化学
醛脱氢酶
细胞生物学
酶
生物
受体
植物
发芽
作者
Youshun Xu,Yuan Qiao-zhen,Shengchuan Cao,Sumei Cui,Li Xue,Xin Song,Lu Zheng,Rong Xu,Qiuhuan Yuan,Ruijian Li
标识
DOI:10.1016/j.bbrc.2020.06.075
摘要
Oxidized low-density lipoprotein (ox-LDL)-mediated NLRP3 inflammasome activation is crucial in atherosclerosis (AS) initiation and progression. Aldehyde dehydrogenase 2 (ALDH2) has been reported to display protective effects during AS development; however, the underlying mechanisms are largely unknown. Here we investigate the role of ALDH2 in ox-LDL-induced NLRP3 inflammasome priming and activation. We treated RAW264.7 murine macrophages with ox-LDL with or without ALDH2 activator Alda-1 and measured NLRP3 inflammasome priming and activation, ALDH2 protein expression and enzyme activity, IL-1β release, and DNA damage. It was found that ox-LDL impaired ALDH2 activity and induced NLRP3 inflammasome priming and activation. Alda-1 inhibited both of the priming and activation steps of NLRP3 inflammasome as well as subsequent cell pyroptosis and attenuated ROS and 4-HNE levels in ox-LDL-treated macrophages. Taken together, ALDH2 activation inhibits priming and activation of NLRP3 inflammasome via reducing oxidative stress, which suggests that ALDH2 may be a potential target for anti-inflammatory therapies in AS treatment.
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