Betaine-palmitate reduces acetylsalicylic acid-induced gastric damage in rats

Citation
I. Zollei et al., Betaine-palmitate reduces acetylsalicylic acid-induced gastric damage in rats, SC J GASTR, 36(8), 2001, pp. 811-816
Citations number
31
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
ISSN journal
00365521 → ACNP
Volume
36
Issue
8
Year of publication
2001
Pages
811 - 816
Database
ISI
SICI code
0036-5521(200108)36:8<811:BRAAGD>2.0.ZU;2-P
Abstract
Background: Acetylsalicylic acid (ASA)-induced gastric injury is reduced wh en ASA is administered along with phosphatidylcholine. The hydrolysis of en dogenous phosphatidylcholine leads to the production of betaine, which may participate in the maintenance of cellular homeostasis. The present aims we re to investigate the effects of exogenous betaine and its palmitic acid co mplex (betaine-palmitate) in the protection of the gastric mucosa in ASA-in duced subacute damage. Methods: Repeated doses of ASA were given intragastr ically to male Wistar rats. Control rats were given vehicle only, while tre ated animals were challenged with ASA or with ASA along with betaine, palmi tic acid or betaine-palmitate. The gastric mucosa was examined after 3 days and the nature of any microscopic mucosal injury was assessed by histology . The extent of macroscopic damage, changes in permeability (assessed by Ev ans blue method) and tissue ATP concentrations were determined in separate series. Results: ASA induced a significant fall in the ATP content of the m ucosa, which was not affected by the other drugs used in the study. However , the ASA-induced mucosal permeability increase could be completely reverse d by betaine-palmitate supplementation. The extent of severity of the macro scopic and microscopic lesions was 33% and 2.45, respectively, for ASA, as compared with 15% and 2.2 for betaine, 14% and 1.9 fur palmitic acid and 3% and 1.4 for betaine-palmitate. Conclusions: Betaine-palmitate affords a si gnificant protective effect against ASA-induced injury, without influencing the ATP synthesis, and this suggests that the defence is due to its abilit y to prevent secondary damage.