缺血后处理对大鼠再灌注损伤肺细胞凋亡的影响

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／n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一2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L／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／Bel．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。

Effects of ischemic postconditioning on pneumocyte apoptosis after lung ischemia/reperfusion injury in rats

Objective： To investigate the effects of ischemic postconditioning （IPostC） on pneumocyte apoptosis after lung ischemia/ reperfusion injury in rats. Methods： Adult male SD rats were randomly divided into 3 groups based upon the intervention （ n = 8） ： control group （C）, lung ischemicl reperfusion group （LIR）, LIR ＋ IPostC group （IPostC）. At the end of the experiment , blood specimens drawn from the arteria carotis were tested for the content of malondialdehyde （MDA）, the activity of superoxide dismutase （ SOD）and myeloperoxidase （MPO）; the pneumocyte apoptosis index （M） was achieved by terminal deoxynucleotidyl transferase mediated dUTP nick end abehng （TUNEL） ; the expression ofBcl-2, Bax protein in lung tissue was accessed by quantitative immanohistochemistry （IHC） and Bcl-2, Bax mR- NA by RT-PCR. Results： IPostC could significantly attenuate the MDA level, MPO activity and improve SOD activity in blood serum which was comparable to I/R and significantly reduced the number of TUNEL-positive cells compared with I/R group, expressed as AI （ % total nu- clei） from（ 39.0 ＋ 3.46 ）to（ 8.0 _＋ 0.88）（ P 〈 0.01 ）. The protein and mRNA expression of Bcl-2 and Bax showed that IPO significantly atten- uated the isehemia/reperfusion-upregulated expression of Bax protein but improved the expression of Bcl-2 that improved the Bcl-2/Bax ratio （ P 〈 0.01 ）. Conclusion： IPostC may attenuate pneumocyte apoptosis in LIRI by up-regulating expression of Bcl-2/Bax ratio and by inhibit- ing oxidant generation and neutmphils filtration.