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Vol. 292, Issue 1, 22-30, January 2000
Division of Clinical Pharmacology, Medizinische Klinik, Klinikum
Innenstadt, University of Munich, Germany
The specific type IV phosphodiesterase inhibitor rolipram is a potent
suppressor of tumor necrosis factor-
(TNF) synthesis. We examined
the efficacy of rolipram for the prevention and treatment of
experimental colitis. To induce colitis, BALB/c mice received 5%
dextran sulfate sodium in their drinking water continuously for up to
11 days. Colitis was quantified by a clinical activity score assessing
weight loss, stool consistency, and rectal bleeding (range from 0 to
4); by colon length; by a semiquantitative histologic score (range from
0 to 6); and by detecting TNF concentration in colonic tissue by
enzyme-linked immunosorbent assay. In a first protocol, rolipram (10 mg/kg b.wt./day i.p.) was started on the same day as dextran sulfate
sodium. Rolipram reduced the clinical activity of colitis (score
1.1 ± 0.3) compared with mice that did not receive rolipram
(2.4 ± 0.4; P = .041). Rolipram also partially reversed the reduction of colon length (without rolipram, 12.4 ± 0.3 cm; with rolipram, 15.4 ± 0.7 cm;
P = .004) and improved the histologic score
(1.5 ± 0.6 in rolipram-treated mice versus 4.6 ± 0.5;
P = .020). Rolipram suppressed colonic tissue TNF
concentrations. The beneficial effect of rolipram was confirmed in a
second protocol in which dextran sulfate sodium exposure was
discontinued on day 7 and rolipram was administered from day 8 through
day 15. These three series of experiments on a total of 153 mice
documented the efficacy of rolipram in both the prevention and
treatment of experimental colitis.
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