Department of VIP General Surgery, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China.
Inflammation. 2015 Feb;38(1):424-32. doi: 10.1007/s10753-014-0047-3.
Intestinal ischemia reperfusion (IR) causes injury of distant critical organs. Remote intestinal ischemic preconditioning (IP) may confer the cytoprotection in critical organs including lung. The authors hypothesized that intestinal IP would be a prophylactic factor in the prevention of distant lung injury induced by IR. Rats were randomly divided into IR, IP, and Sham (S) group. Compared with IR group in the serum and lung tissue, MPO, MDA, TNF-α, and IL-1 levels were significantly decreased in the IP group. Following the same pattern, NO level in the serum and lung tissue was significantly increased in the IP group. And intestinal IP markedly abolished lung injury scores in contrast to IR group. Moreover, intestinal IP significantly attenuated caspase-3 expression, leading to the low expression of Bax and the high expression of Bcl-2. The present study showed that intestinal IP ameliorates the capacity of anti-oxygen free radical, inhibits the release of pro-inflammatory cytokines and alleviates apoptosis in IR-induced lung injury in rats. Intestinal IP may provide a novel prophylactic strategy for treatment of IR-induced lung injury.
肠缺血再灌注（IR）会导致远处重要器官损伤。远程肠缺血预处理（IP）可能会在包括肺在内的重要器官中提供细胞保护作用。作者假设肠 IP 是预防 IR 引起的远处肺损伤的一个预防因素。大鼠随机分为 IR、IP 和 Sham（S）组。与 IR 组相比，IP 组血清和肺组织中的 MPO、MDA、TNF-α 和 IL-1 水平明显降低。同样的模式下，IP 组血清和肺组织中的 NO 水平明显升高。与 IR 组相比，肠 IP 显著减轻了肺损伤评分。此外，肠 IP 显著抑制了 caspase-3 的表达，导致 Bax 的低表达和 Bcl-2 的高表达。本研究表明，肠 IP 改善了抗氧自由基的能力，抑制了促炎细胞因子的释放，并减轻了 IR 诱导的大鼠肺损伤中的细胞凋亡。肠 IP 可能为治疗 IR 诱导的肺损伤提供一种新的预防策略。
