缺血后处理对小鼠肠缺血再灌注所致急性肺损伤保护作用中炎症介质的影响

目的:探讨缺血后处理对于肠缺血再灌注所致急性肺损伤保护作用及其机制.方法:健康雄性C57小鼠36只,随机分为如下3组:假手术组(S组,n=12)、缺血再灌注组(I/R组,n=12)、缺血后处理+缺血再灌注组(IPO+I/R组,n=12).采用小鼠肠缺血再灌注模型及缺血后处理模型,光镜下观察肺组织病理改变,检测肺水肿程度,每组半数小鼠取血检测肺血管通透性以检测肺功能改变,半数小鼠取血检测血清促炎因子TNF-α、IL-6,及抗炎因子IL-10的含量.结果:I/R组肺组织损伤程度明显增高(P＜0.05),肺水肿程度增加(P＜0.05),肺血管通透性增强(P＜0.05),I/R组血清促炎因子TNF-α、IL-6含量较之于C组显著增高(P＜0.05),抗炎因子IL-10的含量较之于C组显著降低(P＜0.05).进行缺血后处理后,IPO组较I/R组TNF-α、IL-6显著降低(P＜0.05),但仍高于C组(P＜0.05).IL-10较I/R组显著增高(P＜0.05).结论:肠缺血后处理的节律刺激干预可减轻肠缺血再灌注所致肺损伤.其保护作用机制可能为增加抗炎因子IL-10表达、抑制促炎因子TNF-α、IL-6表达,进而减轻肺损伤.

Changes of Inflammatory Factors in Protection Effect of Ischemic Postconditioning on Acute Lung Injury Induced by Intestinal Ischemia-Reperfusion

Objective: To investigate the protective effect of ischemic postconditioning(IPO) on acute lung injury induced by intestinal ischemia-reperfusion in mouse.Methods: Thirty C57 mice were divided equally and randomly into three groups as control group(n=12),ischemia-reperfusion group(I/R group,n=12),and ischemic postconditioning group(IPO group,n=12).Pulmonary microvascular permeability and the degree of pulmonary edema was evaluated to assess the lung function.Lung tissue sections were taken for light microscopic observation.Serum TNF-α,IL-6,and IL-10 levels were determined by ELISA.Results: Compared with that respectively in control group,lung tissue injuries in I/R group were more severe,mean wet/dry weight ratio and permeation index of lung was significantly higher,the expression levels of TNF-α and IL-6 were significantly higher,while the expression of IL-10 in I/R group was significantly lower(all P<0.05).After IPO treatment,the degree of lung tissue injuries reduced,the mean wet/dry weight ratio and permeation index of lung was significantly lower,and the expression of TNF-α and IL-6 in IPO group was significantly lower,and the expression of IL-10 was significantly higher than in I/R group(P<0.05).Conclusion: IPO can alleviate the acute lung injury induced by intestinal ischemia-reperfusion.The mechanism is correlated to the enhancement of IL-10 and the inhibition of TNF-α and IL-6.