Glutamine relieves oxidative stress through PI3K/Akt signaling pathway in DSS-induced ulcerative colitis mice
نویسندگان
1 College of Basic Medicine, the Shaanxi University of Chinese Medicine, Xianyang, Shaanxi 712046, P.R. China
2 College of Basic Medicine, the Shaanxi University of Chinese Medicine, Xianyang, Shaanxi 712046, P.R. China
3 Departments of General Surgery, the Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang 712020, Shaanxi, P.R. China
4 Department of Liver Diseases, the Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, Shaanxi 712020, P.R. China
5 Medical Experiment Center, the Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, 712046, P.R. China
6 Medical Experiment Center, the Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, 712046, P.R. China
doi
10.22038/ijbms.2020.39815.9436چکیده
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.