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.