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目的:探讨缺血后处理对再灌注损伤肺细胞凋亡的影响。方法:健康雄性SD大鼠24只,随机分为对照组(C组)、缺血/再灌注组(I/R组)和缺血后处理组(IPostC组)(n=8)。对比观察各组血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活力及含量变化,原位缺口末端标记法(TUNEL)检测肺组织细胞凋亡情况,免疫组化及RT-PCR法检测肺组织中Bax、Bcl-2蛋白和基因的表达。结果:I/R组与C组相比,MDA含量、MPO活力明显升高,SOD活力明显下降(均P<0.01),肺组织原位细胞凋亡检测示I/R组凋亡指数(AI)(39.03±3.46)显著高于C组(2.88±0.34),Bcl-2/Bax比值在蛋白和基因水平明显降低(均P<0.01);IPostC组与I/R组相比MDA含量显著降低(P<0.05),MPO活力显著降低(P<0.01),SOD活性升高(P<0.01),AI为8.03±0.88显著低于I/R组,并能明显升高Bcl-2/Bax比值(均P<0.01)。结论:缺血后处理通过减轻脂质过氧化反应及中性粒细胞聚集,降低Bax/Bcl-2比值,使肺组织细胞凋亡减少,从而有效地减轻肺缺血/再灌注损伤。
Objective: To investigate the effect of ischemic postconditioning on lung cell apoptosis after reperfusion injury. Methods: Twenty - four healthy male SD rats were randomly divided into control group (C group), ischemia / reperfusion group (I / R group) and ischemic postconditioning group (IPostC group) (n = 8). The changes of malondialdehyde (MDA), superoxide dismutase (SOD) and myeloperoxidase (MPO) in serum were observed and compared. The apoptosis of lung tissue was detected by TUNEL The expression of Bax and Bcl-2 protein and gene in lung tissue were detected by immunohistochemistry and RT-PCR. Results: Compared with group C, the content of MDA and the activity of MPO in I / R group were significantly increased, while the activity of SOD in I / R group was significantly decreased (all P <0.01). Apoptosis index in lung tissue of I / R group showed AI ) (39.03 ± 3.46) was significantly higher than that in group C (2.88 ± 0.34), and the ratio of Bcl-2 / Bax was significantly lower at both protein and gene level (all P <0.01); MDA content in IPostC group was significantly lower than that in I / R group (P <0.05). The activity of MPO decreased significantly (P <0.01) and the activity of SOD increased (P <0.01). The AI of 8.03 ± 0.88 was significantly lower than that of I / R group and significantly increased the ratio of Bcl-2 / Bax (All P <0.01). CONCLUSION: Ischemic postconditioning can reduce lung ischemia / reperfusion injury by reducing lipid peroxidation and neutrophil aggregation, decreasing Bax / Bcl-2 ratio and decreasing apoptosis in lung tissue.