南方医科大学学报 ›› 2013, Vol. 33 ›› Issue (02): 299-.

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甘草总黄酮对慢性浅表性胃炎大鼠胃粘膜损伤的保护作用

林晓春,陈育尧,白殊同,郑君,佟丽   

  • 出版日期:2013-02-20 发布日期:2013-02-20

Protective effect of licoflavone on gastric mucosa in rats with chronic superficial gastritis

  • Online:2013-02-20 Published:2013-02-20

摘要: 目的研究甘草总黄酮对慢性浅表性胃炎大鼠胃粘膜损伤的保护作用,探讨其相关药理机制。方法采用0.02%氨水合并
饥饱失常刺激制备大鼠慢性浅表性胃炎模型,模型复制成功后动物随机分为模型对照组、维酶素对照组及甘草总黄酮高、中、低
剂量组,连续灌胃给药30 d。采用HE染色观察胃组织病理学变化;阿利新蓝-糖蛋白结合法(AB-PAS)染色,检测胃粘膜上皮细
胞粘蛋白合成、分泌功能;ELISA法测定血清中前列腺素E2(PGE2)含量;胃体部、幽门部微循环血流量评价胃微循环状况。结
果与正常对照组比较,浅表性胃炎模型组大鼠胃黏膜损伤率、胃组织病理学评分、粘蛋白含量显著改变;与模型对照组比较,试
药组血清PGE2 水平显著升高,上皮细胞粘蛋白指数及酸性粘蛋白指数提高,上皮细胞粘蛋白分泌功能增强和黏膜屏障完整性
得到恢复,大鼠胃黏膜损伤率显著下降。同时,胃微循环血流量改善。结论甘草总黄酮抑制慢性浅表性胃炎大鼠胃粘膜损伤,
保护和修复损伤的粘膜组织,这种作用与提高PGE2水平相关。

Abstract: Objective To evaluate the protective effect of licoflavone on gastric mucosa in rats with chronic superficial gastritis
and explore the possible mechanism. Methods SD rat models of chronic superficial gastritis was established by intragastric
administration of 0.02% ammonia and long-term irregular diet. The rat models were then randomized into model group,
vitacoenzyme group and 3 licoflavone groups of high, medium, and low doses. After 30 days of treatment, the gastric
histopathology, mucosal lesions, scanning electron microscopy, mucin function production by the gastric mucosa epithelial
cells, serum PGE2 level and gastric microcirculation were assessed to evaluate the protective effect of licoflavone on gastric
mucosa. Results Compared with normal control rats, the rat models of chronic superficial gastritis showed significantly higher
gastric mucosal injury rate, histopathological scores and gastric mucin content. Licoflavone significantly ameoliorated gastric
pathology and increased serum PGE2 level, enhanced acidic mucin secretion by the epithelial cells, and improved gastric
microcirculation in the rat models. Conclusion Licoflavone feeding suppresses gastric mucosa injury, protects and restores the
injured mucosa in rats with chronic superficial gastritis, and these effects are related with the up-regulation of serum PGE2
level.