【摘要】：目的:探討重組人白介素-10(rhIL-10)對大鼠肺缺血再灌注損傷的保護作用及可能機制。方法:顯微鏡下夾閉左肺動靜脈和左主支氣管建立單肺缺血再灌注模型。72只Wistar大鼠隨機分為對照組(Control組)、缺血再灌注組(IR組)、rhIL-10藥物干預(yù)組(rhIL-10組),每組分為缺血45min、再灌注60、120min 3個時間點。每個時間點8只,共24只。按上述時間點處死收集標(biāo)本,檢測血漿TNF-α、丙二醛(MDA)水平,觀察肺組織病理變化。結(jié)果:各組MDA在缺血45min時差異無統(tǒng)計學(xué)意義(P0.05),再灌注60min和120min時IR組明顯升高,而rhIL-10組雖較Control組升高,但明顯低于IR組(P0.05)。與Control組比較,IR組缺血45min時TNF-α水平明顯升高(P0.05),rhIL-10組無明顯變化(P0.05)。再灌注60min和120min時IR組TNF-α水平較Control組明顯升高(P0.05),而rhIL-10組雖較Control組顯著升高(P0.05),但明顯低于IR組(P0.05)。肺病理提示肺泡間隔及肺泡內(nèi)炎性細(xì)胞浸潤,肺泡腔內(nèi)大量炎性細(xì)胞滲出、出血,且隨著再灌注時間的延長,損傷加重。rhIL-10組病理損傷均較IR組為輕。結(jié)論:rhIL-10可能通過抑制氧自由基生成、中性粒細(xì)胞浸潤、TNF-α反應(yīng)對肺缺血再灌注損傷起保護作用。
[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- 偽 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- 偽 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- 偽 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- 偽 reaction.
【作者單位】： 山西醫(yī)科大學(xué)附屬第二醫(yī)院胸外科;
【分類號】：R363

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