Impact of colonic mucosal lipoxin A4 synthesis capacity on healing in rats with dextran sodium sulfate-induced colitis
•Disease severity and mucosal lipoxin A4 synthesis were determined in rat colitis model.•5-Aminosalycylic had beneficial effects most prominent in the acute phase.•Misoprostol had favorable effects most marked in the healing phase.•Misoprostol caused a marked increase in mucosal lipoxin A4 synthesis...
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Veröffentlicht in: | Prostaglandins & other lipid mediators 2015-09, Vol.121 (Pt A), p.63-69 |
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Sprache: | eng |
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Zusammenfassung: | •Disease severity and mucosal lipoxin A4 synthesis were determined in rat colitis model.•5-Aminosalycylic had beneficial effects most prominent in the acute phase.•Misoprostol had favorable effects most marked in the healing phase.•Misoprostol caused a marked increase in mucosal lipoxin A4 synthesis capacity.•Misoprostol therapy is efficacious in experimental colitis.
Ulcerative colitis is a chronic inflammatory disease of the colon. This study evaluates the role of colonic mucosal lipoxin A4 (LXA4) synthesis in an experimental rat model of dextran sodium sulfate (DSS)-induced colitis. Wistar rats were randomly assigned to four groups: healthy controls, DSS-induced colitis with no or vehicle therapy, misoprostol or 5-aminosalicylic acid (5-ASA) therapy groups. Disease severity and colonic mucosal LXA4 synthesis was assessed specifically during the acute phase (day 5), chronic phase (day 15) and healing phases (day 19).
Both misoprostol and 5-ASA reduced histopathologic score during the acute phase and reduced disease activity score at the healing phase. In addition, misoprostol reduced histopathologic score and colon weight/length ratio during the healing phase. Only misoprostol therapy increased colonic mucosal LXA4 synthesis. Furthermore, LXA4 levels correlated negatively with disease progression (R=−0.953). Collectively, our findings suggest that misoprostol-induced LXA4 synthesis may be favorable for the healing of ulcerative colitis. |
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ISSN: | 1098-8823 |
DOI: | 10.1016/j.prostaglandins.2015.04.001 |