W2021 Involvement of Corticotropin-Releasing Factor (CRF)/CRF2 Receptors in Pathogenesis of Ischemia/Reperfusion-Induced Intestinal Lesions in Rats

Nakamori, Yuka; Komatsu, Yoshino; Kotani, Tohru; Takeuchi, Koji

doi:10.1016/s0016-5085(09)63578-2

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2009

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“…Kokkotou et al [35] recently reported that CRFR2-null mice developed reduced the severity of intestinal inflammation following luminal exposure to Clostridium difficile toxin A, and this effect was recapitulated by pretreatment with astressin 2B, suggesting the mediation of inflammatory responses by CRF/CRFR2. We also observed recently that Ucn I aggravated the intestinal ulcerogenic response to ischemia/reperfusion, together with an increase of MPO activity, in an astressin 2B-inhibitable manner [51]. Thus, it is possible that CRF might worsen the tissue injury via the CRFR2, if the motility does not play any role in the pathogenic mechanism.…”

Section: Discussionmentioning

confidence: 73%

Urocortin Prevents Indomethacin-Induced Small Intestinal Lesions in Rats Through Activation of CRF2 Receptors

et al. 2009

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These results suggest that urocortin 1 prevents indomethacin-induced small intestinal lesions, and that this action is mediated by the activation of CRFR2 and is functionally associated with the suppression of the intestinal hypermotility response caused by indomethacin. It is assumed that endogenous CRF contributes to the maintenance of the mucosal defensive ability of the small intestine against indomethacin through the activation of CRFR2.

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Section: Discussionmentioning

confidence: 73%