PGE_2在内毒素诱导的幼鼠急性胃黏膜损伤中的变化及PAF受体拮抗剂对其影响  

Change of prostaglandin E_2 and effect of platelet activating factor antagonist on prostaglandin E_2 in endotoxin-induced acute gastric mucosal injury in young rats

作　　者：刘春英[1] 王丽杰[1] 孙梅[1] 赵恂[2] 胡月[1] 赵雅娟[1] 李军[1] 

机构地区：[1]中国医科大学第二临床学院儿科,辽宁省沈阳市110004 [2]中国医科大学实验技术中心二部,辽宁省沈阳市110001

出　　处：《世界华人消化杂志》2006年第2期163-166,共4页World Chinese Journal of Digestology

摘　　要：目的:探讨前列腺素E2(PGE2)在内毒素(LPS) 腹腔注射(ip)诱导的幼鼠急性胃黏膜损伤中的保护作用．方法:18日龄Wistar大鼠,随机分为对照组、 LPS组、PAF受体拮抗剂预防组和治疗组四组.用内毒素(E coli O55:B5脂多糖)5 mg／kg ip 制备幼年大鼠内毒素血症模型,同等量生理盐水ip为对照组,于注射后1．5,3,6,24,48． 72 h处死动物,大体及光学显微镜下观察胃黏膜损伤情况,用放射免疫方法测定胃黏膜 PGE2浓度．观察分别于内毒素ip前和注射后 0．5h应用血小板活化因子(PAF)受体拮抗剂 BN52021(GinkgolideB)5 mg/kg ip对胃黏膜损伤和胃黏膜PGE2浓度影响．结果:内毒素组6h胃黏膜损伤最重,黏膜表面可见大片糜烂、出血、条索状坏死,光镜下上皮脱落,黏膜内有出血,核碎裂、固缩,凋亡小体出现;应用PAF受体拮抗剂后黏膜表面上皮仅见充血水肿,光镜下损伤仅限于黏膜上皮:内毒素组6h胃黏膜PGE2浓度最低,此时 PGE2浓度在LPS组(134．5±9.3μg／L)与对照组 (245．1±8．9 μg／L)间差异显著(P<0．01);在PAF 受体拮抗剂预防组(304．4±15．0μg／L)、PAF 受体拮抗剂治疗组(315．9±43．7 μg／L)与LPS 组(134．5±9．3 μg／L)间均差异显著(P<0．01); PAF受体拮抗剂预防组(304．4±15．0μg／L)和治疗组(315．9±43．7μg／L)与对照组(245．1± 8．9μg/L)间差异显著(P<0．05)．结论:内毒素血症时胃黏膜PGE2下降,PAF受体拮抗剂可以改善这种PGE2下降;PGE2对内毒素造成的幼鼠急性胃黏膜损伤有保护作用．AIM： To investigate the protective effect of prostaglandin E2 （PGE2） in endotoxin-induced acute gastric mucosal injury in young rats. METHODS： Eighteen-day old Wistar rats were randomly divided into normal control, model, platelet activating factor （PAF） antagonist prevention and treatment groups. The model of endotoxemia of young rats was established by intraperitoneal injection of endotoxin （5 mg/kg E coli O55：B5 lipopolysaccharide, LPS）. The rats in PAF prevention and treatment group were administered with PAF antagonist 0.5 h before and after modeling, respectively. The animals were killed 1.5, 3, 6, 24, 48, and 72 h after LPS injection. The pathological changes of gastric mucosa were observed by hematoxylin-eosin （HE） staining. The content of PGE2 was measured by radioimmunoassay method. RESULTS： The pathological changes of gastric mucosa were significant 6 h after LPS injection. Erosion, bleeding and necrosis of gastric mucosa were observed. Swelled epithelial cells and developing degeneration were also observed. However, no remarkable changes occurred in both PAF antagonist groups. In model group, the level of PGE2 in gastric mucosa were significantly lower than that in the control （134.5 ± 9.3 μg/L vs 245.1 ± 8.9 μg/L, P 〈 0.01） 6 h after LPS injection. In PAF antagonist prevention and treatment groups, the levels of PGE2 were markedly higher than those in the model and control group （304.4 ± 15.0, 315.9 ± 43.7 μg/L vs 134.5 ± 9.3, 245.1 ± 8.9 μg/L, P 〈 0.01 or P 〈 0.05） 6 h after LPS injection. CONCLUSION： The level of PGE2 in gastric mucosa is significantly decreased in endotoxemia, but it can be improved by PAF antagonist. PGE2 has protective effect against LPS-induced acute gastric mucosal injury in young rats.

关 键 词：胃黏膜损伤 内毒素 前列腺素E2 血小板活 化因子 PAF受体拮抗剂 

分 类 号：R573[医药卫生—消化系统]