肾缺血再灌注损伤中蛋白激酶C对巨噬细胞的影响

Influence of protein kinase C on macrophages in renal ischemia-reperfusion injury

缺血再灌注损伤是器官移植不可避免的反应过程,其病理生理机制包括细胞凋亡、氧自由基生成、免疫系统活化、微血管功能障碍等。其中先天免疫是机体防御的第一道防线,也是关键环节,而巨噬细胞是肾脏缺血性先天免疫早期重要的起动子,在缺血再灌注损伤中发挥双剑作用。因此,在早期减轻巨噬细胞的浸润是目前的研究热点。而蛋白激酶C抑制剂能通过多途径作用减少移植肾内的巨噬细胞浸润,但目前具体机制尚不完全清楚。

Ischemia-reperfusion injury （IRI） is inevitable for organ transplantation, and its pathophysiological mechanisms include apoptosis, generation of reactive oxygen species （ROS）, innate immune system activation, microvas- cular dysfunction. The innate immune system is the first line of defense, also a critical component of organ transplanta- tion. Macrophages are the critical early initiator of innate immunity in the kidney, which play a dual role in renal isch- emia-reperfusion injury. Therefore, how to reduce macrophage infiltration is a hotspot of ischemia-reperfusion injury. Protein kinase C inhibitors can reduce macrophage infiltrate in the renal allografts through multiple pathways, but how it works is still unclear.