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作 者:刘琳娜[1] 丁士刚[2] 贾淑娟[1] LIU Linna;DING Shigang;JIA Shujuan(Department of Gastroenterology, Peking University Shougang Hospital, Beijing 100144;Department of Gastroenterology, Peking University Third Hospital, Beijing)
机构地区:[1]北京大学首钢医院消化科,100144 [2]北京大学第三医院消化科
出 处:《胃肠病学》2020年第12期731-734,共4页Chinese Journal of Gastroenterology
摘 要:背景:长期服用阿司匹林可造成不同程度的胃黏膜损伤。铝碳酸镁可通过多种机制对胃黏膜损伤发挥保护作用。目的:通过体外实验探讨铝碳酸镁对阿司匹林相关胃黏膜损伤的保护作用及其可能机制。方法:选取人胃黏膜上皮细胞株GES-1,设置正常对照组、损伤组和保护组,后两组加入阿司匹林9 mmol/L共培养,保护组进一步予0.6 mg/mL铝碳酸镁干预。培养12 h后,使用倒置生物显微镜和透射电子显微镜观察细胞形态学变化,MTT实验和流式细胞术检测细胞存活和凋亡情况,蛋白质组学技术筛选、鉴定损伤组与保护组差异表达蛋白。结果:与损伤组相比,保护组GES-1细胞结构相对完整,细胞存活率高、凋亡率低,差异均有统计学意义(P<0.05);T复合蛋白1β亚基(TCP-1β)和硫氧还蛋白依赖性过氧化物还原酶3(PRX3)表达上调,两种蛋白分别与蛋白质的折叠和组装、细胞骨架功能以及抗氧化应激有关。结论:铝碳酸镁可通过促增殖、抗凋亡减轻阿司匹林相关胃黏膜损伤,其机制可能与改善细胞内蛋白质结构和功能、抗氧化应激等有关。Background:Long-term use of aspirin can cause varying degrees of gastric mucosal injuries.Hydrotalcite may play a protective role on gastric mucosal injuries through multiple mechanisms.Aims:To investigate the protective effect of hydrotalcite on aspirin-induced gastric mucosal injury and its possible mechanism in an in vitro study.Methods:Human gastric mucosal epithelial cell line GES-1 was selected and divided into three groups:normal control group,injury group and protection group.GES-1 cells in the latter two groups were co-cultured with aspirin(9 mmol/L),and cells in the protection group was further treated with hydrotalcite(0.6 mg/mL)after aspirin administration.After culturing for 12 hours,morphology of GES-1 cells was observed by inverted microscope and transmission electron microscope.Cell proliferation and apoptosis were assessed by MTT assay and flow cytometry,respectively.Proteomics was used to identify the differentially expressed proteins between injury group and protection group.Results:Compared with the injury group,GES-1 cells in the protection group remained in a relatively intact structure with higher survival rate and lower apoptosis rate(P<0.05).Proteomics revealed that the expressions of T-complex protein 1 subunit beta(TCP-1β)and thioredoxin-dependent peroxide reductase 3(PRX3),which were related with protein folding and assembly,cytoskeleton function,and antioxidative stress,were up-regulated in GES-1 cells in the protection group.Conclusions:Hydrotalcite can reduce the aspirin-induced gastric mucosal injury via promoting cell proliferation and inhibiting apoptosis.Improvement of the structure and function of intracellular proteins and antioxidative stress might be implicated in its cytoprotective effect.
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