Publication: Administration of L-arginine reduces the delay of the healing process caused by ibuprofen.
Implication of COX and growth factors expression
Authors
Sánchez-Fidalgo, S. ; Martín-Lacave, Inés ; Illanes, M. ; Bruseghini, L. ; Esteras, A. ; Motilva, V.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The objective of the present study has been
to advance knowledge of the gastric role played by the
amino acid L-Arginine (L-Arg) in the evolution of a
chronic gastric ulcer. In order to clarify it, L-Arg alone
or together with Ibuprofen have been administrated in an
experimental acetic acid chronic ulcer, analysing
characteristic parameters of an active curative process,
such as PGE2 production, COX expression, and also
angiogenesis, proliferation/apoptosis and growth factors
expression. Our results reveal that L-Arg is favourable in
the healing process improving the curative course.
Ibuprofen caused a delay in ulcer healing, more evident
14 days after ulcer induction; COX-2 expression was
increased at the 7th day although no signal of protein
could be detected after 14 days; PGE2 production was
inhibited in intact and ulcerated areas at both times
assayed. In contrast, treatment with L-Arg reduced the
delay of the lesion, the increment in COX-2 expression
induced by Ibuprofen, and was able to maintain PGE2
levels similar to the control group after 14 days.
Additionally, the histological study showed that the
healing effects of L-Arg might be associated with an
increased angiogenesis and FGF-2 expression. These
actions could be considered key factors in the healing
response associated with L-Arg administration.
However, the proliferation study assayed with the
PCNA-immunostaining method did not reveal significant differences, as the same as the apoptosis
analysis. In conclusion, the coupling of L-Arg to
Ibuprofen is an attractive alternative to Ibuprofen
administration alone because it not only attenuates but
also improves the evolution of chronic lesions through
mechanisms that implicate endogenous PG and FGF-2-
associated pathways, which allow an increase of
angiogenesis process.
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