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Effect of folic acid supplementation on oxidative gastric mucosa damage and acid secretory response in the rat

OBJECTIVE: This study investigated the antioxidative and antisecretory properties of folic acid in the rats’ stomach. MATERIALS AND METHODS: Male Wistar rats were treated with 2 mg/kg diet of folic acid for 21 days. Gastric ulceration was induced by indomethacin, scored, and assayed to determine the...

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Autores principales: Ajeigbe, K. O., Olaleye, S. B., Oladejo, E. O., Olayanju, A. O.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3195131/
https://www.ncbi.nlm.nih.gov/pubmed/22022004
http://dx.doi.org/10.4103/0253-7613.84976
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author Ajeigbe, K. O.
Olaleye, S. B.
Oladejo, E. O.
Olayanju, A. O.
author_facet Ajeigbe, K. O.
Olaleye, S. B.
Oladejo, E. O.
Olayanju, A. O.
author_sort Ajeigbe, K. O.
collection PubMed
description OBJECTIVE: This study investigated the antioxidative and antisecretory properties of folic acid in the rats’ stomach. MATERIALS AND METHODS: Male Wistar rats were treated with 2 mg/kg diet of folic acid for 21 days. Gastric ulceration was induced by indomethacin, scored, and assayed to determine the concentration of total protein, mucus, malondialdehyde (MDA), catalase (CAT) and superoxide dismutase (SOD) in homogenized samples. Normal saline and Ranitidine treated group served as negative and positive control, respectively. Basal and stimulated acid secretion was measured by continuous perfusion method. RESULT: Indomethacin caused severe damage to the rats’ stomach with an ulcer index of 4.32 ± 0.13, increase in MDA concentration and reduction in the concentration of protein, mucus, catalase and superoxide dismutase (P < 0.001). Pre-treatment with folic acid prevented the formation of ulcers by 32%, and attenuated the inhibition of mucus by 14%, CAT, 51% and SOD, 150%. Ranitidine afforded 56% prevention in ulcer formation with 67%, 55% and 78% attenuation of the inhibition of mucus, CAT and SOD, respectively, by indomethacin. While indomethacin-induced lipid peroxidation was attenuated by 58% reduction in MDA concentration on pretreatment with folic acid, Ranitidine offered 65% reduction. Basal and stimulated acid secretions were significantly reduced in the treated when compared with control animals. Folic acid produced a 21% reduction in the basal acid output when compared with the control animals (P < 0.05), and 140% reduction in histamine-induced acid response. CONCLUSION: The results indicate the gastroprotective activity of folic acid due its antioxidative and anti-secretory properties.
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spelling pubmed-31951312011-10-21 Effect of folic acid supplementation on oxidative gastric mucosa damage and acid secretory response in the rat Ajeigbe, K. O. Olaleye, S. B. Oladejo, E. O. Olayanju, A. O. Indian J Pharmacol Short Communication OBJECTIVE: This study investigated the antioxidative and antisecretory properties of folic acid in the rats’ stomach. MATERIALS AND METHODS: Male Wistar rats were treated with 2 mg/kg diet of folic acid for 21 days. Gastric ulceration was induced by indomethacin, scored, and assayed to determine the concentration of total protein, mucus, malondialdehyde (MDA), catalase (CAT) and superoxide dismutase (SOD) in homogenized samples. Normal saline and Ranitidine treated group served as negative and positive control, respectively. Basal and stimulated acid secretion was measured by continuous perfusion method. RESULT: Indomethacin caused severe damage to the rats’ stomach with an ulcer index of 4.32 ± 0.13, increase in MDA concentration and reduction in the concentration of protein, mucus, catalase and superoxide dismutase (P < 0.001). Pre-treatment with folic acid prevented the formation of ulcers by 32%, and attenuated the inhibition of mucus by 14%, CAT, 51% and SOD, 150%. Ranitidine afforded 56% prevention in ulcer formation with 67%, 55% and 78% attenuation of the inhibition of mucus, CAT and SOD, respectively, by indomethacin. While indomethacin-induced lipid peroxidation was attenuated by 58% reduction in MDA concentration on pretreatment with folic acid, Ranitidine offered 65% reduction. Basal and stimulated acid secretions were significantly reduced in the treated when compared with control animals. Folic acid produced a 21% reduction in the basal acid output when compared with the control animals (P < 0.05), and 140% reduction in histamine-induced acid response. CONCLUSION: The results indicate the gastroprotective activity of folic acid due its antioxidative and anti-secretory properties. Medknow Publications 2011 /pmc/articles/PMC3195131/ /pubmed/22022004 http://dx.doi.org/10.4103/0253-7613.84976 Text en Copyright: © Indian Journal of Pharmacology http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Short Communication
Ajeigbe, K. O.
Olaleye, S. B.
Oladejo, E. O.
Olayanju, A. O.
Effect of folic acid supplementation on oxidative gastric mucosa damage and acid secretory response in the rat
title Effect of folic acid supplementation on oxidative gastric mucosa damage and acid secretory response in the rat
title_full Effect of folic acid supplementation on oxidative gastric mucosa damage and acid secretory response in the rat
title_fullStr Effect of folic acid supplementation on oxidative gastric mucosa damage and acid secretory response in the rat
title_full_unstemmed Effect of folic acid supplementation on oxidative gastric mucosa damage and acid secretory response in the rat
title_short Effect of folic acid supplementation on oxidative gastric mucosa damage and acid secretory response in the rat
title_sort effect of folic acid supplementation on oxidative gastric mucosa damage and acid secretory response in the rat
topic Short Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3195131/
https://www.ncbi.nlm.nih.gov/pubmed/22022004
http://dx.doi.org/10.4103/0253-7613.84976
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