米诺环素
炎症体
药理学
促炎细胞因子
小胶质细胞
医学
缺血
神经炎症
化学
免疫学
炎症
内科学
抗生素
生物化学
作者
Yunnan Lu,Guodong Xiao,Weifeng Luo
出处
期刊:Neuroimmunomodulation
[S. Karger AG]
日期:2016-01-01
卷期号:23 (4): 230-238
被引量:71
摘要
<b><i>Objective:</i></b> Minocycline, a tetracycline antibiotic, has shown anti-inflammatory effects in cerebral ischemia and neurodegenerative disease; however, the molecular mechanisms underlying this effect have not been clearly identified. Since NLRP3 inflammasome activation controls the maturation and release of proinflammatory cytokines, especially interleukin-1β (IL-1β) and IL-18 in ischemia stroke, we suppose that minocycline may be involved in the regulation of NLRP3 inflammasome activation. <b><i>Methods:</i></b> We investigated the effects of minocycline on NLRP3 inflammasome activation using the transient middle cerebral artery occlusion (tMCAO) mouse model and an in vitro oxygen-glucose deprivation/reoxygenation injury model in BV2 microglial cells. <b><i>Results:</i></b> We found that minocycline administrated 1 h after reperfusion can improve neurological disorder, reduce infarct volume, and alleviate cerebral edema. Meanwhile, we showed that minocycline prevented the activation of microglias and attenuated NLRP3 inflammasome signaling after tMCAO injury. Furthermore, we found that the pretreatment of minocycline significantly inhibited signal 1 and signal 2 of NLRP3 inflammasome activation in BV2 cells. <b><i>Conclusion:</i></b> We demonstrated that minocycline can ameliorate ischemia-induced brain damage via inhibiting NLRP3 inflammasome activation.
科研通智能强力驱动
Strongly Powered by AbleSci AI