摘要
近年来研究发现细胞间黏附分子-1和单核细胞趋化蛋白-1等炎症因子、核因子-κB及中性粒细胞、单核/巨噬细胞等炎症细胞参与了急性缺血性肾损伤的发生发展,抑制急性缺血性肾损伤时肾脏的炎症反应具有保护肾脏作用。
Investigations in recent years have confirmed that intercellular adhesion molecule-l, nuclear factor kappa B, monocyte chemoattractant protein-l, neutrophils, macrophages and lymphocytes were involved in the development of acute ischemic kidney injury (AIKI). Inhibition of renal inflammation could protect kidney from AIKI.
出处
《生命的化学》
CAS
CSCD
北大核心
2008年第6期755-758,共4页
Chemistry of Life
关键词
急性缺血性肾损伤
缺血再灌注
炎症
acute ischemic kidney injury
ischemia/reperfusion
inflammation