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后处理对缺血再灌注损伤鼠肺EGR-1表达的影响

发布时间:2018-11-06 11:16
【摘要】:目的:研究后处理对在体缺血再灌注损伤大鼠肺EGR-1表达的影响,并分析其可能的肺保护作用机制。 方法:建立大鼠在体肺脏缺血再灌注损伤模型,将24只SD大鼠随机分为假手术(Sham)组、缺血再灌注(I/R)组和缺血后处理(IPostC)组,每组8只。在体大鼠I/R损伤模型制备完成后,阻断左肺门,终止血供及通气,造成左肺缺血,达预定时间后松开阻断带恢复血供及通气形成再灌注。Sham组只游离左侧肺门、套阻断带但不阻断,等待3h后直接取标本;I/R组缺血1h后再灌注2h; IPostC组缺血1h后给予重复三次的5min灌注和5min缺血的后处理,继以恢复血供及通气再灌注1.5h。3组实验结束后均留取左侧肺组织:取部分制成10%的组织匀浆,用于测定髓过氧化物酶(MPO)的含量;留取小块肺组织测定肺湿/干重比(W/D),并在光镜下观察肺组织的病理变化;RT-PCR法检测其余左肺组织中EGR-1 mRNA及IL-1βmRNA的表达量。 结果:三组间各项检测指标比较,差异均有显著性(P0.05)。①W/D值:与Sham组(4.4935±0.4171)比较,I/R组(6.6513±0.3820)明显升高(P0.05);而IPostC组(5.5151±0.2693)则明显低于I/R组(P0.05)。②肺组织中MPO的含量:与Sham组(1.1847±0.2636)比较,I/R组(2.2732±0.5593)明显升高(P0.05);而与I/R组相比,IPostC组(1.6317±0.2015)明显降低(P0.05)。③肺组织IL-1βmRNA的表达量:与Sham组(0.2308±0.0083)比较,I/R组(0.5500±0.0281)明显升高(P0.05);而与I/R组比较,IPostC组(0.3661±0.0080)明显降低(P0.05)。④肺组织EGR-1 mRNA的表达量:与Sham组(0.2975±0.0289)比较,I/R组(0.6147±0.0152)明显升高(P0.05);而与I/R组相比,IPostC组(0.4680±0.0166)明显降低(P0.05)。⑤病理形态学观察:Sham组肺间质及肺泡基本完整,未见炎症细胞浸润;I/R组均出现不同程度的肺泡水肿,毛细血管破裂出血,肺间质增宽并有水肿,炎症细胞浸润,肺泡内有较多血液成分渗出;IPostC组肺间质轻度水肿,少量炎症细胞浸润,肺泡内有少量血液成分渗出。 结论:后处理能够明显减轻鼠肺缺血再灌注损伤,从而起到肺保护作用。其机制可能与其抑制缺血再灌注损伤鼠肺组织中EGR-1及IL-1β的表达从而减轻肺组织炎症反应有关。
[Abstract]:Aim: to study the effect of post-treatment on the expression of EGR-1 in the lung of rats with ischemia-reperfusion injury in vivo and to analyze its possible protective mechanism. Methods: 24 SD rats were randomly divided into sham-operated (Sham) group, ischemia-reperfusion (I / R) group and post-ischemic (IPostC) group (8 rats in each group). After the model of I / R injury was made in rats, the left hilus was blocked, blood supply and ventilation were terminated, left lung ischemia was caused, and the blood supply was restored and ventilated reperfusion was formed after the release of the blocking band. The Sham group only left the left pulmonary hilum. The specimens were collected directly after 3 hours. In I / R group, 1 h after ischemia and 2 h after reperfusion; After 1 hour of ischemia, IPostC group was treated with repeated 5min perfusion and 5min ischemia, then the left lung tissue was retained after blood supply recovery and ventilation reperfusion in 1.5h.3 group: 10% tissue homogenate was obtained. To determine the content of myeloperoxidase (MPO); Lung wet / dry weight ratio (W / D) was measured in small lung tissue and the pathological changes of lung tissue were observed under light microscope. The expression of EGR-1 mRNA and IL-1 尾 mRNA in other left lung tissues were detected by RT-PCR method. Results: there were significant differences among the three groups (P0.05). 1W/D value: compared with Sham group (4.4935 卤0.4171), I / R group (6.6513 卤0.3820) significantly increased (P0.05); The content of MPO in lung tissue in IPostC group (5.5151 卤0.2693) was significantly lower than that in I / R group (P0.05). Compared with Sham group (1.1847 卤0.2636), I / R group (2.2732 卤0.5593) was significantly higher (P0.05). Compared with I / R group, IPostC group (1.6317 卤0.2015) significantly decreased the expression of IL-1 尾 mRNA in lung tissue: compared with Sham group (0.2308 卤0.0083), I / R group (0.5500 卤0.0281) significantly increased the expression of IL-1 尾 mRNA (P0.05). Compared with I / R group, IPostC group (0.3661 卤0.0080) significantly decreased the expression of EGR-1 mRNA in lung tissue (P0.05). Compared with Sham group (0.2975 卤0.0289), I / R group (0.6147 卤0.0152) significantly increased the expression of EGR-1 mRNA (P0.05). Compared with I / R group, IPostC group (0.4680 卤0.0166) was significantly lower than that of I / R group (P0.05). 5 Pathomorphological observation showed that interstitial and alveolar infiltration was almost intact in Sham group, and no inflammatory cell infiltration was found. In the I / R group, alveolar edema, capillary rupture and hemorrhage, pulmonary interstitial enlargement and edema, inflammatory cell infiltration and blood component exudation in the alveoli were found in all cases. In IPostC group, the interstitial edema was mild, a small amount of inflammatory cells infiltrated, and a few blood components exudated in the alveoli. Conclusion: post-treatment can significantly reduce lung ischemia-reperfusion injury and thus play a protective role in lung injury. The mechanism may be related to its inhibition of the expression of EGR-1 and IL-1 尾 in the lung tissue of rats with ischemia-reperfusion injury, thereby reducing the inflammatory response of the lung tissue.
【学位授予单位】:遵义医学院
【学位级别】:硕士
【学位授予年份】:2011
【分类号】:R363

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相关期刊论文 前2条

1 梁贵友,牛义民,刘达兴,徐刚,蔡庆勇;内源性一氧化氮抗兔肺缺血再灌注损伤作用及其机制探讨[J];四川大学学报(医学版);2005年02期

2 邹树;田伏洲;汤礼军;黎冬暄;汪涛;石力;;早期生长反应基因-1与大鼠急性胰腺炎合并肺损伤[J];四川医学;2007年05期



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