Amb motiu del tancament d'estiu, la validació de documents es reprendrà a partir del 28 d'agost de 2026. Disculpeu les molèsties.
Con motivo del cierre de verano, la validación de documentos se reanudará a partir del 28 de agosto de 2026. Disculpad las molestias
Due to the summer closure, document validation will resume starting August 28, 2026. We apologize for any inconvenience.

Files

694714.pdf (4.83 MB)

Document type

Article

Version

Published version

Publication date

2020-01-08

Publication license

cc-by (c) Sánchez, Aroha B. et al., 2020
Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/161984

Study of Melatonin as Preventive Agent of Gastrointestinal Damage Induced by Sodium Diclofenac

Journal Title

Authors

Director/Tutor

Journal ISSN

Volume Title

Related resource

https://doi.org/10.3390/cells9010180

Abstract

: Safety profile of nonsteroidal anti‐inflammatory drugs (NSAIDs) has been widely studied and both therapeutic and side effects at the gastric and cardiovascular level have been generally associated with the inhibitory effect of isoform 1 (COX‐1) and 2 (COX‐2) cyclooxygenase enzymes. Now there are evidences of the involvement of multiple cellular pathways in the NSAIDs‐mediated‐gastrointestinal (GI) damage related to enterocyte redox state. In a previous review we summarized the key role of melatonin (MLT), as an antioxidant, in the inhibition of inflammation pathways mediated by oxidative stress in several diseases, which makes us wonder if MLT could minimize GI NSAIDs side effects. So, the aim of this work is to study the effect of MLT as preventive agent of GI injury caused by NSAIDs. With this objective sodium diclofenac (SD) was administered alone and together with MLT in two experimental models, ex vivo studies in pig intestine, using Franz cells, and in vivo studies in mice where stomach and intestine were studied. The histological evaluation of pig intestine samples showed that SD induced the villi alteration, which was prevented by MLT. In vivo experiments showed that SD altered the mice stomach mucosa and induced tissue damage that was prevented by MLT. The evaluation by quantitative reverse transcription PCR (RT‐qPCR) of two biochemical markers, COX‐2 and iNOS, showed an increase of both molecules in less injured tissues, suggesting that MLT promotes tissue healing by improving redox state and by increasing iNOS/NO that under non‐oxidative condition is responsible for the maintenance of GI‐epithelium integrity, increasing blood flow and promoting angiogenesis and that in presence of MLT, COX‐2 may be responsible for wound healing in enterocyte. Therefore, we found that MLT may be a preventive agent of GI damages induced by NSAIDs. Keywords: melatonin; NSAIDs; gastric injuries; antioxidant

Subject

Melatonina, Antioxidants, Agents antiinflamatoris, Tracte gastrointestinal

Subject (English)

Melatonin, Antioxidants, Antiinflammatory agents, Gastrointestinal system

Citation

Collections

Articles publicats en revistes (Bioquímica i Fisiologia)
Articles publicats en revistes (Farmàcia, Tecnologia Farmacèutica i Fisicoquímica)

Citation

SÁNCHEZ, Aroha B., et al. Study of Melatonin as Preventive Agent of Gastrointestinal Damage Induced by Sodium Diclofenac. Cells. 2020. Vol. 9, num. 1, pags. 180-197. ISSN 2073-4409. [consulted: 15 of August of 2026]. Available at: https://hdl.handle.net/2445/161984

Export metadata

JSON - METS

Share record