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Title: [Role and related mechanism of resolvin D1 in lung ischemia reperfusion injury in rats].
Author: Xia J, Xue JY, Du J, Wu GW, Hu XT, Zhao QF.
Journal: Zhonghua Yi Xue Za Zhi; 2019 Apr 09; 99(14):1111-1115. PubMed ID: 30982262.
Abstract:
Objective: To investigate the role and related mechanism of resolvin D1 (RvD1) in lung ischemia-reperfusion injury (LIRI) in rats. Methods: Forty male Sprague-Dawley rats, 7-8 weeks, weighing 220-280 g, were divided into 4 groups using a random number table method: sham operation group, lung ischemia reperfusion control group, normal saline group, and RvD1 group. The rat model of LIRI was produced by 45 min of occlusion of the left hilum of lungs followed by 150 min reperfusion. In sham group, no blocking of the left hilum of lung after thoracotomy; Normal saline 2 ml/kg and RvD1 100 μg/kg were injected respectively at 10 min of reperfusion in normal saline group and RvD1 group. Blood samples were collected from the femoral vein for determination of interleukin (IL)-6, tumor necrosis factor (TNF)-α, soluble inter-cell adhesion molecules (sICAM-1) concentrations at 150 min of reperfusion. The rats were sacrificed after collection of blood samples and then lung tissues were taken for observation of the pathological changes and for measurement of lung wet/dry weight ratio (W/D). The the contents of malondialdehyde (MDA), monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-2 and the activity of myeloperoxidase (MPO) in lung tissues were determined. The protein relative expression of nuclear factor (NF)-κB in lung tissues was detected by Western blot. Lung tissue cell apoptosis was detected with TUNEL method. Results: The plasma level of IL-6, TNF-α, sICAM-1 in normal saline group and RvD1 group were significantly higher than those in the Sham group [(110±7), (100±4) vs (72±3) ng/L, (151±8), (153±6) vs (104±5) ng/L, (2 690±133), (2 760±167) vs (1 953±125) ng/L]. Besides, NF-κB protein relative expression level of lung tissues up-regulated [(0.681±0.033), (0.664±0.024) vs (0.292±0.011)] (all P<0.05). The W/D, apoptosis index, MDA, MCP-1, MIP-2 contents and MPO activity in lung ischemia reperfusion control group, normal saline group and RvD1 group were significantly higher than those in the Sham group [(5.92±0.31), (5.85±0.24), (5.06±0.08) vs (4.14±0.10), (32.9±1.5)%, (31.9±1.3)%, (17.7±1.8)% vs (8.1±0.6)%, (72.1±2.3), (66.7±3.7), (34.0±1.4) vs (22.0±0.8) nmol/mg, (3.99±0.28), (3.86±0.25), (2.66±0.16) vs (1.47±0.17) pg/mg, (9.45±0.53), (9.68±0.62), (7.62±0.22) vs (4.70±0.41) pg/mg, (3.01±0.18), (2.92±0.19), (1.58±0.11) vs (0.98±0.07) U/g] (all P<0.05). The plasma levels of the cytokines mentioned above, the W/D, the apoptosis index, MDA, MCP-1, MIP-2 contents and MPO activity in RvD1 group were significantly lower than those in the lung ischemia reperfusion control group [(63±4) vs (110±7) ng/L, (90±8) vs (151±8) ng/L, (1 835±182) vs (2 690±133) ng/L, (5.06±0.08) vs (5.92±0.31), (17.7±1.8)% vs (32.9±1.5)%, (34.0±1.4) vs (72.1±2.3) nmol/mg, (2.66±0.16) vs (3.99±0.28) pg/mg, (7.62±0.22) vs (9.45±0.53) pg/mg, (1.58±0.11) vs (3.01±0.18) U/g]. Besides, NF-κB protein relative expression level of lung tissues down-regulated [(0.313±0.012) vs (0.681±0.033)] (all P<0.05). Inflammatory cell infiltration in LIRI groups increased significantly, while it was significantly reduced in RvD1 group. Conclusion: RvD1 can effectively alleviate the tissue damage caused by lung ischemia-reperfusion through down-regulating NF-κB expression, relieving inflammatory reaction and oxidative stress, reducing apoptosis in rats. 目的： 探讨消退素D1（RvD1）在大鼠肺缺血再灌注损伤（LIRI）中的作用及其机制。 方法： 清洁级7~8周龄健康雄性SD大鼠40只，体质量220~280 g，采用随机数字表法均分为4组：假手术组、LIRI对照组、生理盐水组、RvD1组。所有动物采用夹闭左肺门45 min，再灌注150 min的方法制备大鼠LIRI模型。假手术组打开胸腔后动脉夹仅穿过左肺门不进行阻断；LIRI对照组不注射药物；生理盐水组和RvD1组于再灌注10 min时分别注入生理盐水2 ml/kg和RvD1 100 μg/kg。于再灌注150 min时取各组大鼠股静脉检测血浆白细胞介素（IL）-6、肿瘤坏死因子（TNF）-α、可溶性细胞间黏附分子-1（sICAM-1）浓度。取血后处死大鼠取肺组织，HE染色观察肺组织病理变化，测定肺湿干重比（W/D）；测定丙二醛（MDA）、单核细胞趋化蛋白-1（MCP-1）、巨噬细胞炎性蛋白-2（MIP-2）含量及髓过氧化物酶（MPO）活性；采用Western印迹法检测肺组织核因子（NF）-κB蛋白相对表达量；同时采用TUNEL法检测肺组织细胞凋亡指数（AI）。 结果： LIRI对照组、生理盐水组血浆IL-6、TNF-α、sICAM-1浓度均显著高于假手术组[（110±7）、（100±4）比（72±3）ng/L，（151±8）、（153±6）比（104±5）ng/L，（2 690±133）、（2 760±167）比（1 953±125）ng/L]，肺组织NF-κB相对表达量显著上调[（0.681±0.033）、（0.664±0.024）比（0.292±0.011）]（均P<0.05）；LIRI对照组、生理盐水组、RvD1组肺组织W/D、AI、MDA、MCP-1、MIP-2含量和MPO活性均显著高于假手术组[（5.92±0.31）、（5.85±0.24）、（5.06±0.08）比（4.14±0.10），（32.9±1.5）%、（31.9±1.3）%、（17.7±1.8）%比（8.1±0.6）%，（72.1±2.3）、（66.7±3.7）、（34.0±1.4）比（22.0±0.8）nmol/mg，（3.99±0.28）、（3.86±0.25）、（2.66±0.16）比（1.47±0.17）pg/mg，（9.45±0.53）、（9.68±0.62）、（7.62±0.22）比（4.70±0.41）pg/mg，（3.01±0.18）、（2.92±0.19）、（1.58±0.11）比（0.98±0.07）U/g]（均P<0.05）。RvD1组血浆IL-6、TNF-α、sICAM-1浓度，肺组织W/D、AI、MDA、MCP-1、MIP-2含量和MPO活性显著低于LIRI对照组[（63±4）比（110±7）ng/L，（90±8）比（151±8）ng/L，（1 835±182）比（2 690±133）ng/L，（5.06±0.08）比（5.92±0.31），（17.7±1.8）%比（32.9±1.5）%，（34.0±1.4）比（72.1±2.3）nmol/mg，（2.66±0.16）比（3.99±0.28）pg/mg，（7.62±0.22）比（9.45±0.53）pg/mg，（1.58±0.11）比（3.01±0.18）U/g]，NF-κB相对表达量显著下调[（0.313±0.012）比（0.681±0.033）]（均P<0.05）。LIRI各组肺组织炎性细胞浸润明显增多，而RvD1组肺组织炎性细胞浸润明显减轻。 结论： RvD1可下调NF-κB蛋白表达，缓解炎症反应和抑制氧化应激，减少细胞凋亡，有效减轻大鼠LIRI。.

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