医学
地塞米松
内科学
细胞凋亡
细胞周期蛋白D1
肿瘤坏死因子α
蛋白激酶B
内分泌学
药理学
胃粘膜
谷氨酰胺
胃
生物化学
化学
细胞周期
癌症
氨基酸
作者
Ahmed M El-Lekawy,Dalaal M. Abdallah,Hanan S. El‐Abhar
标识
DOI:10.1097/mpg.0000000000002474
摘要
Alanylglutamine (AG) is a dipeptide that fuels enterocytes and has a coadjuvant role during gut healing. The current study aimed to investigate the potential ulcer-healing effect of AG in indomethacin-induced gastropathy.Animals (n = 10 rats/group) were randomly allocated into 5 groups. Gastric ulcerated rats were administered AG, AG + dexamethasone, or pantoprazole after indomethacin exposure.Comparable to pantoprazole, AG inhibited H-KATPase pump, and elevated the pH of gastric juice. Moreover, the dipeptide increased the serum/mucosal contents of glucagon-like peptide-1 (GLP-1), pS473-Akt, and cyclin-D1. On the contrary, AG abated serum tumor necrosis factor-α and gastric mucosal content of pS45-β catenin, pS9-GSK3β, pS133-CREB, pS536-NF-κB, H2O2, claudin-1, and caspase-3. The administration of dexamethasone before AG hampered its effect on almost all the measured parameters.AG confers its antiulcerogenic/antisecretory potentials by repressing the proton pump to increase the gastric juice pH via boosting p-CREB, p-Akt, p-GSK-3β, and GLP-1. Also, it inhibits apoptosis through suppressing nuclear factor-kappa B/tumor necrosis factor-α/H2O2/claudin-1 cue. This trajectory contributes to loosen the tight junction priming AG-mediated GLP-1/β-catenin/cyclin-D1 that results in pronounced increase in gastric mucosa proliferation. Therefore, the crosstalk between multiple pathways orchestrates the action of AG against gastric ulceration.
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