【摘要】 目的考察姜辣素抗小鼠胃溃疡作用并初步探讨其作用机制。方法采用幽门结扎法致小鼠胃溃疡模型和阿司匹林致胃溃疡模型,判定胃黏膜损伤指数;收集胃液,测其胃液量,总酸度,胃蛋白酶活性及游离黏液量,胃壁结合黏液量及6-酮前列腺素F1α(6-keto-prostaglandin F1α,6-keto-PGF1α)的含量。结果姜辣素能减少幽门结扎和阿司匹林致胃黏膜损伤指数,对胃液分泌有抑制作用,可以显著降低胃液总酸度。但对胃蛋白酶无显著影响。对胃液中游离黏液和胃壁结合黏液的分泌有显著地促进作用。并能显著增加6-keto-PGF1α的含量。结论姜辣素具有一定的抗胃溃疡的作用,其机制可能与增加前列腺素E2(prostaglandin E2,PGE2)合成有关。更多还原

【Abstract】 Objective To explore the anti-gastric ulcer effect of gingerols in mice and its mechanism. Methods The gastric ulcer models were established in mice by pyloric ligation and aspirin in order to determine the gastric mucosal injury index.The volume of gastric juice,total acidity,the activity of pepsin,the amount of free mucus,the amount of gastric wall mucus and the amount of 6-keto-PGF1α were measured by collecting gastric juice. Results Gingerols(73,145,290 mg·kg-1)significantly reduced the gastric mucosal injury index induced by pyloric ligation in mice.Gingerols(73,145,290 mg·kg-1)could inhibit the excessive secretion of gastric juice.Gingerols(145,290 mg·kg-1)could significantly reduce the total acidity of gastric juice.Gingerols had no significant effect on the activity of pepsin.Gingerols(145,290 mg·kg-1)could significantly increase the amount of free mucus.Gingerols(73,145,290 mg·kg-1)significantly reduced the gastric mucosal injury index induced by aspirin in mice.Gingerols(290 mg·kg-1)could significantly increase the amount of gastric wall mucus.Gingerols(73,145,290 mg·kg-1)could significantly increase the amount of 6-keto-PGF1α. Conclusions Gingerols play a protective role in gastric mucosa injury,and its mechanism may be related to increase the amount of PGE2.更多还原