A
Akiko Tanaka
Researcher at Kyoto Pharmaceutical University
Publications - 103
Citations - 2684
Akiko Tanaka is an academic researcher from Kyoto Pharmaceutical University. The author has contributed to research in topics: Small intestine & Rofecoxib. The author has an hindex of 27, co-authored 102 publications receiving 2488 citations. Previous affiliations of Akiko Tanaka include Kobe Pharmaceutical University.
Papers
More filters
Journal ArticleDOI
Up-regulation of cyclooxygenase-2 by inhibition of cyclooxygenase-1: a key to nonsteroidal anti-inflammatory drug-induced intestinal damage.
TL;DR: The results suggest that the intestinal ulcerogenic property of NSAID is not accounted for solely by inhibition of COX-1 and requires inhibition ofCOX-2 as well, and this may be a key to NSAID-induced intestinal damage.
Journal ArticleDOI
Inhibition of both COX-1 and COX-2 is required for development of gastric damage in response to nonsteroidal antiinflammatory drugs
TL;DR: The results suggest that the gastric ulcerogenic property of conventional NSAIDs is not accounted for solely by COx-1 inhibition and requires the inhibition of both COX-1 andCOX-2.
Journal ArticleDOI
Roles of enterobacteria, nitric oxide and neutrophil in pathogenesis of indomethacin-induced small intestinal lesions in rats.
TL;DR: It is strongly suggested that enterobacterial translocation in the mucosa is the first step required for activation of various factors such as iNOS/NO and neutrophils, all involved in the pathogenesis of indomethacin-induced intestinal lesions.
Journal ArticleDOI
Role of cyclooxygenase (COX)-1 and COX-2 inhibition in nonsteroidal anti-inflammatory drug-induced intestinal damage in rats: relation to various pathogenic events.
TL;DR: Indomethacin decreased mucosal prostaglandin (PG)E2 content and caused damage in the intestine within 24 h, accompanied by an increase in intestinal contractility, bacterial numbers, myeloperoxidase (MPO) and inducible nitric-oxide synthase (iNOS) activity, and intestinal motility, which explains why intestinal damage occurs only when bothCOX-1 and COX-2 are inhibited.
Journal ArticleDOI
Pathogenic importance of intestinal hypermotility in NSAID-induced small intestinal damage in rats
TL;DR: The results suggest the pathogenic importance of intestinal hypermotility in the intestinal ulcerogenic response to NSAIDs in rats and show that this event is critical for the occurrence of enterobacterial invasion under PG deficiency, followed by various inflammatory changes and damage in the mucosa.