Droy-Lefaix M T, Drouet Y, Geraud G, Hosford D, Braquet P
IHB/IPSEN Research Laboratories, Paris, France.
Free Radic Res Commun. 1991;12-13 Pt 2:725-35. doi: 10.3109/10715769109145852.
Oxygenated free-radicals appear to play a prominent role in mediating damage associated with gastrointestinal diseases. Production of reactive oxygen metabolites in ischemia-reperfusion involves oxidases found in resident phagocytic cells and microvascular and mucosal epithelial cells. Platelet activating factor (PAF), a phospholipid associated with inflammatory disorders, has been shown to both prime and amplify the release of superoxide anion and hydrogen peroxide from polymorphonuclear neutrophils and macrophages stimulated by FMLP or PMA. To further elucidate the involvement of free radicals in intestinal damage and the potential role of PAF in their production, we examined the effect of superoxide dismutase (SOD) and BN 52021 (ginkgolide B) on ischemia-reperfusion induced damage in the small intestine. The study involved 32 Sprague-Dawley rats (100-200 g) divided into four groups. Three of these groups were subjected to occlusion of the mesenteric artery 30 mins followed by 24 h reperfusion. On 2 groups SOD (15,000 U/kg/iv) and BN 52021 (20 mg/kg/po) were administered 45 mins before arterial occlusion. Following the 24 h reperfusion, the rats were sacrificed after overnight fasting. The jejunum and ileon were removed and fixed for morphological examination. Lesions in the small intestine were quantified. The results showed extensive necrosis, hemorrhage, oedema and neutrophil invasion in the jejunal and ileal mucosa. This injury was significantly reduced by SOD (15,000 U/kg/iv) and BN 52021 (20 mg/kg/po) pretreatment. In conclusion, free-oxygenated radicals appear to mediate reperfusion damage in the small intestine and PAF appears to be involved in the genesis of these toxic products. Thus, SOD and BN 52021 may be considered as protectors against ischemic disorders.
氧化自由基似乎在介导与胃肠道疾病相关的损伤中起重要作用。缺血再灌注过程中活性氧代谢产物的产生涉及驻留吞噬细胞、微血管和粘膜上皮细胞中的氧化酶。血小板活化因子（PAF）是一种与炎症性疾病相关的磷脂，已被证明可引发并放大由FMLP或PMA刺激的多形核中性粒细胞和巨噬细胞中超氧阴离子和过氧化氢的释放。为了进一步阐明自由基在肠道损伤中的作用以及PAF在其产生中的潜在作用，我们研究了超氧化物歧化酶（SOD）和BN 52021（银杏内酯B）对小肠缺血再灌注损伤的影响。该研究涉及32只Sprague-Dawley大鼠（100 - 200克），分为四组。其中三组接受肠系膜动脉闭塞30分钟，随后再灌注24小时。在两组中，在动脉闭塞前45分钟给予SOD（15,000 U/kg/静脉注射）和BN 52021（20 mg/kg/口服）。24小时再灌注后，大鼠禁食过夜后处死。取出空肠和回肠并固定用于形态学检查。对小肠病变进行定量分析。结果显示空肠和回肠粘膜出现广泛坏死、出血、水肿和中性粒细胞浸润。SOD（15,000 U/kg/静脉注射）和BN 52021（20 mg/kg/口服）预处理可显著减轻这种损伤。总之，氧化自由基似乎介导小肠的再灌注损伤，PAF似乎参与了这些毒性产物的产生。因此，SOD和BN 52021可被视为缺血性疾病的保护剂。
