Dehydroevodiamine ameliorates indomethacin-induced gastric injury via inhibition of ERK and p38 signaling pathway |
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| Affiliation: | 1. School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China;2. Department of Pharmacy, the Fifth Medical Center of Chinese PLA General Hospital, Beijing, China;3. China Military Institute of Chinese Medicine, the Fifth Medical Center of Chinese PLA General Hospital, Beijing, China;1. Laboratory of Translational Physiology and Pharmacology, Pharmaceutical Sciences Graduate Program, Vila Velha University (UVV), Vila Velha, ES, Brazil;2. Laboratory of Translational Physiology, Health Sciences Center, Federal University of Espirito Santo (UFES), Vitoria, Brazil;3. Federal Institute of Education, Science and Technology (IFES), Vila Velha, ES, Brazil;1. Division of Physiology, Department of Basic Sciences, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran;2. Division of Pathology, Department of Pathobiology, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran;3. Division of Biochemistry, Department of Basic Sciences, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran |
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| Abstract: | BackgroundDehydroevodiamine (DHE), a pivotal quinazoline alkaloid isolated from Fructus Evodiae (Tetradium ruticarpum (A. Juss.) Hartley), has various pharmacological effects. However, the effect of DHE on gastric injury is still uncharted.PurposeTo clarify the pharmacological effect and mechanism of DHE on gastric injury (GI) induced by indomethacin (IDO).Study designThe gastric injury was induced in rat by oral administration of 5 mg/kg IDO for 7 days. Then the rats were treated with DHE (10, 20, 40 mg/kg, ig) for 7 days.MethodsThe changes of food intake, body weight, gastric pH and general state observation were determined. And HE staining and AB-PAS staining was analyzed. Then, the inflammatory infiltration of gastric tissue was observed through MPO immunohistochemical approach, and the expression of TNF-α, IL-6 and IL-10 were measured. Furthermore, the levels of proteins ERK, p-ERK, P38, p-P38, JNK and p-JNK were determined to elucidate the molecular mechanism of DHE.ResultsDHE alleviated food intake reduction, weight loss and gastric injury induced by IDO and made gastric pH and mucosal thickness return to normal. In addition, DHE could down regulate the expression of MPO, TNF-α and IL-6 and up regulate the expression of IL-10 to reduce the damage induced by inflammatory, and create a healing environment. Furthermore, DHE could significantly inhibit the phosphorylation of ERK and p38 not JNK.ConclusionDHE ameliorated dyspepsia, inflammatory infiltration and tissue damage induced by IDO through ERK and p38 signaling pathways rather than JNK pathway. |
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