中文摘要：

目的探讨黄芪预处理对大鼠小肠缺血再灌注损伤的影响及其抗氧化作用机制。方法健康雄性清洁级Wistar大鼠32只（200～250g），分成假手术组（SH组，仅开腹，n=12）、模型组（M组，缺血再灌注组，n=8）及黄芪预处理组（E组，黄芪＋缺血再灌注损伤组，黄芪20g/kg在实验前3d经腹腔注入，每天1次，n=12）。在小肠缺血前即刻，SH组及E组分别选取4只大鼠，以小肠缺血60min再灌注2h后各组选取8只大鼠，观察各组动物肠黏膜病理学变化，测定小肠黏膜MDA、H2O2与TNF-α含量及SOD与MPO活性，检测小肠黏膜gp91phox及ICAM-1蛋白表达。结果在小肠缺血前即刻，E组的MDA、H2O2含量及gp91^phox表达较SH组明显降低（P〈0．05），SOD活性增加（P〈0．05）。小肠缺血再灌注导致M组Chiu’s评分，IMDA、H2O2与TNF-α含量，MPO活性，gp91phox与ICAM-1蛋白表达较SH组明显增加（P〈0．05）；SOD活性较sH组显著降低（P〈0．05）。与M组比较：E组Chiu’s评分，IMDA、H2O2与TNF-α含量，MPO活性，gp91phox与ICAM-1蛋白表达明显降低（P〈0．05）；SOD活性显著升高（P〈0．05）。结论黄芪预处理能够减轻小肠缺血再灌注损伤，与其提高抗氧化能力有关。

英文摘要：

Objective To investigate the protective role of pretreatment of astragalus membranaceus （AE） in rats with small intestinal ischemia reperfusion injury. Methods Thirty-two healthy male Wistar rats, weighing 200 to 250 g were divided into 3 groups, sham-operation group （ group SH, open the abdomen, with- out ischemia reperfusion, n = 12 ）, model group （group M, 60 min intestinal ischemia followed by 120 min repeffusion, n = 8）, and AE pretreatment group （group E, intraperitoneally injected with 20 g/kg AE once per day for 3 consecutive days prior to isehemia repeffusion injury, n = 12）. The tissue samples of small intestinal mucosa were harvested for pathology evaluation from 4 rats just prior to ischemia from groups SH and E, and 8 rats after intestinal ischemia/reperfusion injury from groups SH, M, and E. The contents of MDA, H2 02 and TNF-ct, and activities of MPO and SOD in the mucosa were measured. Protein expression levels of gp91phox and ICAM-1 in the mucosa were detected by Western blotting. Results At the time-point prior to ischemia, the contents of MDA and H202 and the protein level of gp91 phox were significantly decreased in group E as compared with group SH （P 〈 0. 05 ）, whereas, SOD activity was dramatically higher （P 〈 0. 05 ）. At the time-point after ischemia repeffusion, Chiu＇ s score, contents of MDA, H2O2, arid TNF-ct, activity of MPO, and protein expression of gp91phox and ICAM-1 were significantly increased, while activity of SOD was significantly decreased compared with those indexes in group SH （ P 〈 0.05 ）. Furthermore, AE pretreatment resulted in significant decreases in above increased indexes, while 0. 05）. Conclusion AE pretreatment protects small obvious elevation in above decreased SOD activity （P 〈 intestine mucosa against ischemia-reperfusion injury by enhancing anti-oxidative capacity.