Published in

Bentham Science Publishers, Current Pharmaceutical Design, 8(28), p. 655-660, 2022

DOI: 10.2174/1381612826666200908144053

Links

Tools

Export citation

Search in Google Scholar

Evaluation of Gastroprotective Activity of Linoleic acid on Gastric Ulcer in a Mice Model

This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

Full text: Unavailable

Green circle
Preprint: archiving allowed
Orange circle
Postprint: archiving restricted
Red circle
Published version: archiving forbidden
Data provided by SHERPA/RoMEO

Abstract

Background: Gastric ulcer has been a major cause of morbidity and mortality worldwide, and it has been linked to factors such as nutritional deficiency, smoking, stress, and continuous intake of non-steroidal anti-inflammatory drugs (NSAIDs). The search for new anti-ulcer therapeutic agents has been the subject of several studies. Recently, the gastroprotective effect of Celtis iguanaea has been reported, with linoleic acid (LA) responsible for many of the therapeutic effects of this medicinal plant. Aim: This study aims to investigate the gastroprotective activity and the possible mechanisms in which LA may be involved, through different experimental assays in mice. Methods: The gastroprotective activity LA was evaluated in the ulcer induced by indomethacin, HCl/EtOH, hypothermicrestraint stress and pyloric ligation. For the gastroprotective mechanisms investigation the quantification of the volume (mL), pH and total acidity of gastric secretion were considered. Results: The oral administrations of 25 mg/kg, 50 mg/kg or 100 mg/kg of body weight of LA were capable of protecting the gastric mucosa against HCl/ethanol (10 mL/kg p.o.), and oral administrations of 50 mg/kg LA showed protection from ulcers induced by indomethacin, hypothermic-restraint stress and pyloric ligation. Conclusion: The results of this study show the gastroprotective role of LA in gastric mucosal damage induced by all assayed distresses. The observed gastroprotection possibly occurs due to the mediated increase of mucosal defensive factors.