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目的研究蜂胶水提液(water extract of propolis,WEP)对大鼠肠缺血/再灌注(ischemia-reperfusion,I/R)致肺损伤的影响,并探讨其保护作用机制。方法 32只健康雄性Wistar大鼠随机分为4组:假手术(Sham)组、I/R组、低剂量(100 mg/kg)WEP预处理(WEP100)组和高剂量(200 mg/kg)WEP预处理(WEP200)组。以无创动脉夹夹闭肠系膜上动脉45 min,再灌注2 h建立小肠I/R模型,采集动脉血进行血气分析,测定肺系数判定组织水肿情况,光镜下观察肺组织病理学改变,试剂盒测定肺组织髓过氧化物酶(myeloperoxidase,MPO)活性,免疫组化法和Western blotting检测肺组织核因子-κB p65(nuclear factor-κB p65,NF-κB p65)和细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)表达。结果与I/R组比较,WEP预处理组PaO2升高而PaCO2降低(P<0.05),肺系数减小(P<0.05)且肺组织病理变化减轻;WEP剂量依赖性地抑制肠I/R所致的肺组织MPO活性升高(P<0.05),并下调肺组织NF-κB p65和ICAM-1的表达(P<0.05或P<0.01)。结论蜂胶水提液可减轻肠I/R大鼠肺损伤,其机制可能与抑制NF-κB活化,进而减少ICAM-1介导的中性粒细胞浸润有关。
Objective To investigate the effect of water extract of propolis (WEP) on lung injury induced by intestinal ischemia / reperfusion (I / R) in rats and its protective mechanism. Methods Thirty-two healthy male Wistar rats were randomly divided into 4 groups: Sham group, I / R group, low dose (100 mg / kg) WEP pretreatment group and high dose (200 mg / WEP Pretreatment (WEP200) group. The superior mesenteric artery was occluded for 45 min and then reperfused for 2 h. The arterial blood was collected for blood gas analysis. The lung coefficient was used to determine the tissue edema. The pathological changes of the lung tissue were observed under light microscope. The activity of myeloperoxidase (MPO) in lung tissue was determined. The expression of nuclear factor-κB p65 and intercellular adhesion molecule-1 (NF-κB p65) in lung tissue were detected by immunohistochemistry and Western blotting intercellular adhesion molecule-1, ICAM-1). Results Compared with I / R group, WEP pretreatment group PaO2 increased PaCO2 decreased (P <0.05), lung coefficient decreased (P <0.05) and lung tissue pathological changes alleviated; WEP dose-dependent inhibition of intestinal I / R (P <0.05), and decreased the expression of NF-κB p65 and ICAM-1 in lung tissue (P <0.05 or P <0.01). Conclusion Propolis aqueous extract can relieve lung injury in intestinal I / R rats. The mechanism may be related to the inhibition of NF-κB activation and the decrease of ICAM-1-mediated neutrophil infiltration.