Glutamine relieves oxidative stress through PI3K/Akt signaling pathway in DSS-induced ulcerative colitis mice
- سال انتشار: 1399
- محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 23، شماره: 9
- کد COI اختصاصی: JR_IJBMS-23-9_003
- زبان مقاله: انگلیسی
- تعداد مشاهده: 261
نویسندگان
College of Basic Medicine, the Shaanxi University of Chinese Medicine, Xianyang, Shaanxi ۷۱۲۰۴۶, P.R. China
College of Basic Medicine, the Shaanxi University of Chinese Medicine, Xianyang, Shaanxi ۷۱۲۰۴۶, P.R. China
Department of Liver Diseases, the Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, Shaanxi ۷۱۲۰۲۰, P.R. China
Medical Experiment Center, the Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, ۷۱۲۰۴۶, P.R. China
چکیده
Objective(s): Ulcerative colitis (UC) is a kind of complex immune disease, and a major cause of destruction of intestinal barrier and oxidative stress in this field. In this paper, glutamine (Gln) was believed to offer protection against oxidative stress injury in colitis mice.Materials and Methods: Thirty mice were randomly assigned into control, model, LY294002 (PI3K/Akt inhibitor), Gln, Gln+LY294002 and 5-Aminosalicylic acid (5-ASA) groups. The mice in the experimental group drank 4% dextran sulfate sodium salt (DSS) for 7 consecutive days. The protective effect of Gln on oxidative stress was quantified by keeping colitis mice, involving Phosphatidylinositol-3-kinase (PI3K)/Protein kinase B (Akt)/mammalian target of Rapamycin (mTOR) signaling pathway, with different medications or distilled water through intragastric administration for 10 consecutive days.Results: In vivo administration of Gln, LY294002 or 5-ASA was found to ameliorate the symptoms of colitis in mice, such as reduced growth, loose stools and stool bleeding; protected DSS-induced colitis mice from goblet cell loss, lymphocytosis, mucosal erosion, loss of crypts, and neutrophil infiltration; improved the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-XP); decreased the content of malondialdehyde (MDA); and inhibited the activation of PI3K/Akt signaling pathway.Conclusion: Administration of Gln to the DSS-induced colitis mice led to a clearly reduction in oxidative stress-induced injury. The Gln is confirmed as inhibiting the PI3K/Akt signaling pathway activity.کلیدواژه ها
Colitis, Glutamine, mTOR protein, Oxidative stress, Protein kinase Bاطلاعات بیشتر در مورد COI
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