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目的探讨缺血后处理对在体大鼠肺缺血再灌注损伤的炎症反应的影响。方法将40只SD大鼠随机分成5组:假手术组(C组)、缺血-再灌注组(IR30组、IR120组)、缺血后处理组(IPC30组、IPC120组),通过阻断左肺门建立大鼠在体肺缺血再灌注模型,用免疫组化法测定肺组织中TNF-α,IL-1β的表达水平。结果 TNF-α表达阳性率:C组(4.65±1.09)%,IR30组(19.68±2.47)%,IR120组(29.37±2.45)%,IPC30组(12.31±1.80)%,IPC120组(18.80±2.88)%;IL-1β的表达阳性率:C组(5.22±0.58)%,IR30组(23.90±1.22)%,IR120组(29.57±3.11)%,IPC30组(16.46±2.50)%,IPC120组(21.86±3.40)%。肺组织经缺血再灌注后,与C组相比,IR组TNF-α,IL-1β的表达水平均明显升高(P<0.05或P<0.01),且随着时间的推移有上升趋势;而IPC组与相应时段的IR组相比,表达水平均明显降低(P<0.01)。结论缺血后处理可抑制再灌注鼠肺组织中致炎因子TNF-α和IL-1β的表达,减轻局部炎症反应,对肺组织缺血再灌注损伤起一定的保护作用。
Objective To investigate the effect of ischemic postconditioning on the inflammatory response of lung ischemia-reperfusion injury in rats. Methods Forty Sprague-Dawley rats were randomly divided into 5 groups: sham operation group (C group), ischemia-reperfusion group (IR30 group, IR120 group), ischemic postconditioning group (IPC30 group, IPC120 group) The model of lung ischemia-reperfusion injury was established in the left hilum of rats. The expression of TNF-α and IL-1β in lung tissue was detected by immunohistochemistry. Results The positive rates of TNF-α in C group (4.65 ± 1.09%), IR30 group (19.68 ± 2.47)%, IR120 group (29.37 ± 2.45)%, IPC30 group (12.31 ± 1.80)%, IPC120 group ), The positive rate of IL-1β expression was 5.22 ± 0.58% in C group, 23.90 ± 1.22% in IR30 group, 29.57 ± 3.11% in IR120 group, 16.46 ± 2.50% in IPC30 group, 21.86 ± 3.40)%. Compared with group C, the expression of TNF-α and IL-1β in lung tissue of IR group was significantly increased (P <0.05 or P <0.01) after ischemia-reperfusion, and there was an upward trend with time ; While IPC group and the corresponding period of IR group, the expression levels were significantly lower (P <0.01). Conclusion Ischemic postconditioning can inhibit the expression of inflammatory cytokines TNF-α and IL-1β in the lungs of rats with reperfusion, relieve the local inflammatory reaction and play a protective role on the lung ischemia-reperfusion injury.