After demonstration that cysteamine induced duodenal lesions in gastrectomi
zed rats, while a number of antiulcer drugs mitigated these lesions, it was
shown that one single intrarectal (i.r.) cysteamine application produced s
evere colon lesions in acute studies in rats. Thus, the further focus was o
n the protracted effect of cysteamine challenge (400 mg/kg b.w. i.r.) and t
herapy influence in chronic experiments in female rats. Regularly, cysteami
ne colon lesions were markedly mitigated by ranitidine (10), omeprazole (10
), atropine (10), methylprednisolone (1), sulphasalazine (50; mg/kg), penta
decapeptide BPC 157 (PL-10, PLD-116, 10 mug or 10 ng/kg). Specifically, aft
er 1 or 3 months following initial challenge (cysteamine 400 mg/kg i.r.) in
female rat, the therapy [BPC 157 (PL-10, PLD-116 (10.0 mug or 10.0 ng/kg;
i.g., i.p., i.r.), ranitidine, omeprazole, atropine, methylprednisolone, su
lphasalazine (i.p.)] reversed the protracted cysteamine colon injury: the 1
week-regimen (once daily application) started after 1 month post-cysteamin
e, as well as the 2 weeks-regimen (once daily application), which started a
fter 3 months. The effect on recidive lesion was also tested. These cysteam
ine lesions may reappear after stopping therapy (after stopping therapy for
3 weeks at the end of 2-weeks regimen started in 3 months-cysteamine femal
e rats) in sulphasalazine group, while this reappearance is markedly antago
nized in pentadecapeptide BPC 157 (PL-10, PLD-116)-rats (cysteamine-colon l
esion still substantially low). (C) 2001 Elsevier Science Ltd. All rights r
eserved.