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MECHANISM AND PREVENTION OF CHRONIC COLONIC INFLAMMATION WITH TRINITROBENZENE SULFONIC ACID IN RATS
Author(s) -
Hoshino Hiroshi,
Sugiyama Satoru,
Ohara Atsushi,
Goto Hidemi,
Tsukamoto Yoshihisa,
Ozawa Takayuki
Publication year - 1992
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1992.tb00409.x
Subject(s) - colitis , prostanoid , inflammation , thromboxane b2 , pharmacology , prostaglandin , chemistry , prostaglandin e2 , immune system , prostaglandin e , medicine , immunology , biochemistry , platelet
SUMMARY 1. The role of prostanoids in experimental colitis with trinitrobenzene sulfonic acid (TNBS) in rats was investigated. The effects of cyclosporine A (CsA) on the development of experimental colitis were also examined. 2. Five kinds of prostanoids were detected in rat colonic tissue by high performance liquid chromatography. These were 6‐keto‐prostaglandin (PG) F 1α , PGF 2α , PGE 2 , PGD 2 and thromboxane B 2 . 3. In TNBS‐induced experimental colitis, all prostanoid concentrations except PGD 2 increased, although the time courses differed from each other. 4. Medication with indomethacin markedly reduced prostanoid concentrations in TNBS‐induced colitis. However, indomethacin did not show any effect on damage scores. 5. Cyclosporine A reduced damage scores 14 days after TNBS treatment, and the protective effects were observed, whereas CsA did not affect colonic tissue prostanoid concentrations. 6. Prostanoids might be produced secondarily in the genesis of TNBS‐induced colitis, although they may attenuate the inflammatory response. It was also suggested that CsA was likely to have therapeutic effects on experimental colitis by inhibiting the immune reaction with TNBS, which induced the chronic inflammation.