ROS/TXNIP pathway contributes to thrombin induced NLRP3 inflammasome activation and cell apoptosis in microglia.
ROS/TXNIP pathway contributes to thrombin induced NLRP3 inflammasome activation and cell apoptosis in microglia.
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ROS/TXNIP 通路有助于凝血酶诱导的小胶质细胞中 NLRP3 炎性体激活和细胞凋亡。
DOI：
10.1016/j.bbrc.2017.02.019
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发表时间：
2017-04
期刊：
影响因子：
--
通讯作者：
Cui Guiyun
中科院分区：
文献类型：
--
作者：
Ye Xinchun;Zuo D;an;Yu Lu;Zhang Liang;Tang Jiao;Cui Chengcheng;Bao Lei;Zan Kun;Zhang Zuohui;Yang Xinxin;Chen Hao;Tang Hai;Zu Jie;Shi Hongjuan;Cui Guiyun
There is no effective therapy for intracerebral hemorrhage (ICH) because of poor understanding of the mechanisms of brain injury after hemorrhage. The NLRP3 inflammasome, as a vital component of innate immune system, which is associated with a wide range of human CNS disorders, including ICH. But its detailed mechanisms in ICH remain mainly unclear. In this study, BV2 cells with thrombin exposure were used to investigate the role of NLRP3 inflammasome in thrombin-induced brain injury. We used western blot to detect NLRP3 inflammasome activation and the expression of thioredoxin binding protein (TXNIP), DCFH-DA to investigate intracellular reactive oxygen species (ROS), flow cytometry to analyze apoptosis. Our results showed that ROS inhibitor N-acetyl-l-cysteine (NAC) suppressed the upregulation of intracellular ROS and TXNIP expression. Furthermore, the cell apoptosis and expression of apoptotic protein were significantly attenuated after treatment of thrombin with NAC or NLRP3 antagonist (MCC950). Thrombin activates ROS/TXNIP/NLRP3 signaling in BV2 cells, which may indicate a mechanism that pro-inflammatory and pro-apoptotic contributes to the development of ICH.
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影响因子：
8.7
作者：
Elliott EI;Sutterwala FS
通讯作者：
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影响因子：
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作者：
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11.2
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DOI：
10.1016/j.bbrc.2016.10.007
发表时间：
2016-11-04
影响因子：
3.1
作者：
Ye, Xinchun;Kong, Delian;Hua, Fang
通讯作者：
Hua, Fang