Publication: A COX-2 inhibitor, nimesulide, inhibits chemically-induced rat tongue
carcinogenesis through suppression of cell
proliferation activity and COX-2 and iNOS expression
Authors
Yoshida, K. ; Tanaka, T. ; Kohno, H. ; Sakata, K. ; Kawamori, T. ; Mori, H. ; Wakabayashi, K.
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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 modifying effects of a cyclooxygenase
(cox)-2 selective inhibitor nimesulide on tongue
carcinogenesis were investigated in male F344 rats
initiated with 4-nitroquinoline-1-oxide (4-NQO). The
cell proliferation activity measured by proliferating cell
nuclear antigen (PCNA)-positive index and apoptotic
index, and the immunohistochemical expression of
COX-2, and inducible nitric oxide synthase (iNOS) in
the tongue mucosa or neoplasms were also examined for
mechanistic analysis of modifying effects of nimesulide
on tongue carcinogenesis. All animals except those
treated with nimesulide alone and untreated rats were
given 20 ppm 4-NQO in drinking water for 8 weeks to
induce tongue neoplasms. Starting 1 week after the
cessation of 4-NQO exposure, rats given 4-NQO were
fed the experimental diets containing nimesulide (100
and 400 ppm) for 22 weeks. At week 32, the incidence
of tongue squamous cell carcinoma was significantly
reduced by feeding of the diet containing 400 ppm
nimesulide. Feeding of nimesulide significantly
decreased polyamine content and PCNA-labeling index
in tongue carcinoma. Apoptotic index in tongue
carcinoma was increased by feeding of nimesulide. In
addition, nimesulide feeding reduced COX-2 and iNOS
expression in the tongue dysplasia and neoplasms. These
results suggest that 400 ppm nimesulide in diet, when
given during the promotion phase, exerts
chemopreventive ability against 4-NQO-induced tongue
tumorigenesis through inhibition of cell proliferation
activity in conjunction with modification of COX-2 and
iNOS expression of the target lesions.
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