학술논문
甘草次酸抑制胃溃疡大鼠胃黏膜细胞的凋亡 / Glycyrrhetinic acid inhibits the apoptosis of gastric mucosa cells in gastric ulcer rats
Document Type
Academic Journal
Author
孙俊波; 赵璐; 史素琴; 寇振媛; 刘爱娟; 付婷婷; SUN Jun-bo; ZHAO Lu; SHI Su-qin; KOU Zhen-yuan; LIU Ai-juan; FU Ting-ting
Source
中成药 / Chinese Traditional Patent Medicine. 39(3):462-466
Subject
Language
Chinese
ISSN
1001-1528
Abstract
目的 分析甘草次酸对幽门螺杆菌感染胃溃疡大鼠的影响,并探讨其作用机理.方法 采用乙酸处理后幽门螺杆菌感染法制备胃溃疡大鼠模型,检测不同剂量甘草次酸处理后大鼠溃疡指数以及胃酸、胃蛋白酶活性.同时检测甘草次酸对大鼠胃黏膜组织及体外胃黏膜上皮细胞中B淋巴细胞瘤-2 (BCL2)和天冬氨酸蛋白水解酶-3(Caspase-3)表达、糖原合成酶激酶-3 (GSK3β)活性及细胞凋亡水平的影响.结果 甘草次酸可降低大鼠的溃疡指数以及胃液中胃酸、胃蛋白酶活性.甘草次酸处理后,大鼠胃黏膜组织及体外胃黏膜上皮细胞中凋亡抑制因子BCL2的表达显著增高,而凋亡因子Caspase-3的表达量、激酶GSK3β活性及细胞凋亡水平则明显下降.GSK3β激活剂LY294002作用于细胞后,BCL2水平下调,Caspase-3表达增多,细胞凋亡水平上升.结论 甘草次酸可通过调控GSK3β激酶活性,抑制胃黏膜上皮细胞的凋亡,进而促进幽门螺杆菌感染胃溃疡的愈合.
AIM To explore the effects of glycyrrhetinic acid on the gastric ulcer rats infected by Helicobacter pylori (Hp) and its action mechanism.METHODS Gastric ulcer rat models were induced by acetic acid stress and then followed by Hp infection.After treatment with low and high doses of glycyrrhetinic acid,the ulcer index,gastric acid and proteinase activities in gastric ulcer rats were analyzed.The effects of glycyrrhetinic acid on the expressions of BCL2 and Caspase-3,the GSK3β activity in gastric mucosa and gastric epithelial cells,and the cell apoptosis level were then detected.RESULTS Glycyrrhetinic acid reduced the ulcer index,gastric acid and proteinase activities in rats.Besides,the expression of BCL2 was significantly up-regulated by glycyrrhetinic acid in gastric mucosa and gastric epithelial cells,whereas the expression of Caspase-3,level of cell apoptosis,and GSK3β activity were significantly reduced.After the treatment with GSK3 β activator LY294002,the level of BCL2 was down-regulated,Caspase-3 expression was increased,and the level of cell apoptosis was enhanced.CONCLUSION Glycyrrhetinic acid promotes the healing of gastric ulcer infected by Hp via regulating GSK3β activity and inhibiting apoptosis of gastric epithelial cells.
AIM To explore the effects of glycyrrhetinic acid on the gastric ulcer rats infected by Helicobacter pylori (Hp) and its action mechanism.METHODS Gastric ulcer rat models were induced by acetic acid stress and then followed by Hp infection.After treatment with low and high doses of glycyrrhetinic acid,the ulcer index,gastric acid and proteinase activities in gastric ulcer rats were analyzed.The effects of glycyrrhetinic acid on the expressions of BCL2 and Caspase-3,the GSK3β activity in gastric mucosa and gastric epithelial cells,and the cell apoptosis level were then detected.RESULTS Glycyrrhetinic acid reduced the ulcer index,gastric acid and proteinase activities in rats.Besides,the expression of BCL2 was significantly up-regulated by glycyrrhetinic acid in gastric mucosa and gastric epithelial cells,whereas the expression of Caspase-3,level of cell apoptosis,and GSK3β activity were significantly reduced.After the treatment with GSK3 β activator LY294002,the level of BCL2 was down-regulated,Caspase-3 expression was increased,and the level of cell apoptosis was enhanced.CONCLUSION Glycyrrhetinic acid promotes the healing of gastric ulcer infected by Hp via regulating GSK3β activity and inhibiting apoptosis of gastric epithelial cells.