Role of Sodium Channel PN1 in Ulcerative Colitis
Ulcerative colitis (UC) is an inflammatory disease which involves swelling and ulceration of the mucosa layer of the colon. It has been proposed that inflammation in ulcerative colitis (UC) may in part be caused by a dysregulation of local protective immune mechanisms due to a change in the sodium channel peripheral sodium channel 1 (PN 1) of the gut intrinsic sensory neurons. The aims of this study were to confirm the presence of PN 1 in the submucosa ganglia and to establish a trinitrobenzenesulfonic acid (TNBS) model of colitis, both to prepare for further PNI research on the aged rat as well as the UC rat models. A section of dissected colonic submucosa plexus was stained with the antibodies to PNI and a positive staining, demonstrated the sodium channel's existence in intrinsic sensory neurons. Colitis was induced using TNBS and confirmed through histological assessment of colonic tissue as well as western blotting for inducible nitric oxide synthase (iNOS). The histology clearly showed altered mucosal structure in the TNBS treated rats while the western blots for iNOS showed an upregulation of the substance compared to the controls. These results establish the basis from which other studies examining the PNI sodium channels in the aging as well as UC gut can be performed.
iii, 18 p.
U.S. copyright laws protect this material. Commercial use or distribution of this material is not permitted without prior written permission of the copyright holder.