Does insulin-like growth factor-I partially attenuate colonic damage in rats with experimental colitis induced by oral dextran sulphate sodium?
We conclude that the effects of IGF-I treatment on the colonic epithelium may be mediated directly, whereas the reduced inflammation in the mucosa and submucosa may be mediated by a mechanism other than up-regulation of TGF-beta1-mediated immunosuppression.
These data indicate that targeted toxins induce apoptosis by activating components of the death receptor pathway in a receptor-independent manner.