右美托咪定
p38丝裂原活化蛋白激酶
MAPK/ERK通路
药理学
细胞凋亡
缺血
体内
炎症
再灌注损伤
医学
生物
化学
内科学
细胞生物学
信号转导
镇静
生物化学
生物技术
作者
Xiaoming Liu,Qiuhong Chen,Qian Hu,Zhen Liu,Qiong Wu,Si-Si Liang,Huai‐Gen Zhang,Qin Zhang,Xuekang Zhang
标识
DOI:10.1016/j.yexmp.2020.104444
摘要
Intestinal ischemia-reperfusion (I/R) is a life-threatening condition associated with high morbidity and mortality. Dexmedetomidine (DEX), an agonist of α2-adrenoceptor with sedation and analgesia effect, has recently been identified with protective function against I/R injury in multiple organs. However, the mechanism underlying the beneficial effect of DEX on intestine after I/R injury remained poorly understood. In the present study, using in both in vitro and in vivo models, we found that intestinal I/R injury was associated with the activation of p38 MAPK cascade, while DEX was capable of deactivating p38 MAPK and thus protect intestinal cells from apoptosis by inhibiting p38 MAPK-mediated mitochondrial depolarization and cytochrome c (Cyto C) release. Moreover, through inhibiting p38 MAPK activity, the downstream production of pro-inflammatory cytokines-regulated by NF-κB was also suppressed by DEX treatment, leading to the resolution of I/R-induced inflammation in intestine. In general, our study provided evidence that DEX protected intestine from I/R injury by inhibiting p38 MAPK-mediated mitochondrial apoptosis and inflammatory response.
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