重组人白介素-10对大鼠肺缺血再灌注损伤的保护作用

发布时间：2018-12-18 07:27

【摘要】：目的:探讨重组人白介素-10(rhIL-10)对大鼠肺缺血再灌注损伤的保护作用及可能机制。方法:显微镜下夹闭左肺动静脉和左主支气管建立单肺缺血再灌注模型。72只Wistar大鼠随机分为对照组(Control组)、缺血再灌注组(IR组)、rhIL-10药物干预组(rhIL-10组),每组分为缺血45min、再灌注60、120min 3个时间点。每个时间点8只,共24只。按上述时间点处死收集标本,检测血浆TNF-α、丙二醛(MDA)水平,观察肺组织病理变化。结果:各组MDA在缺血45min时差异无统计学意义(P0.05),再灌注60min和120min时IR组明显升高,而rhIL-10组虽较Control组升高,但明显低于IR组(P0.05)。与Control组比较,IR组缺血45min时TNF-α水平明显升高(P0.05),rhIL-10组无明显变化(P0.05)。再灌注60min和120min时IR组TNF-α水平较Control组明显升高(P0.05),而rhIL-10组虽较Control组显著升高(P0.05),但明显低于IR组(P0.05)。肺病理提示肺泡间隔及肺泡内炎性细胞浸润,肺泡腔内大量炎性细胞渗出、出血,且随着再灌注时间的延长,损伤加重。rhIL-10组病理损伤均较IR组为轻。结论:rhIL-10可能通过抑制氧自由基生成、中性粒细胞浸润、TNF-α反应对肺缺血再灌注损伤起保护作用。
[Abstract]:Aim: to investigate the protective effect of recombinant human interleukin-10 (rhIL-10) on lung ischemia-reperfusion injury in rats and its possible mechanism. Methods: single lung ischemia-reperfusion model was established with left pulmonary arteriovenous occlusion and left main bronchus occlusion under microscope. 72 Wistar rats were randomly divided into control group (Control group), ischemia-reperfusion group (IR group) and rhIL-10 drug intervention group (rhIL-10 group). Each group was divided into ischemia 45 min, reperfusion 60120min 3 time points. Each time point 8, altogether 24. The plasma TNF- 伪 and malondialdehyde (MDA) (MDA) levels were measured and the pathological changes of lung tissue were observed. Results: there was no significant difference in MDA in ischemic 45min group (P0.05). IR group increased significantly during reperfusion 60min and 120min, while rhIL-10 group was higher than Control group, but significantly lower than IR group (P0.05). Compared with Control group, the level of TNF- 伪 in IR group was significantly higher than that in IR group (P0.05), but there was no significant change in rhIL-10 group (P0.05). The level of TNF- 伪 in IR group was significantly higher than that in Control group (P0.05), while that in rhIL-10 group was significantly higher than that in Control group (P0.05), but significantly lower than that in IR group (P0.05). Pulmonary pathology indicated that the alveolar septum and alveolar inflammatory cells infiltrated, a large number of inflammatory cells in alveolar cavity exudated, bleeding, and with the prolongation of reperfusion time, the injury was aggravated. The pathological injury in rhIL-10 group was lighter than that in IR group. Conclusion: rhIL-10 may protect lung ischemia-reperfusion injury by inhibiting oxygen free radical formation, neutrophil infiltration and TNF- 伪 reaction.
【作者单位】：山西医科大学附属第二医院胸外科;
【分类号】：R363

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