Mechanisms of Motility Change on Trinitrobenzenesulfonic Acid-Induced Colonic Inflammation in Mice

Abstract

Ulcerative colitis is an inflammatory bowel disease (IBD) characterized by recurrent episodes of colonic inflammation and tissue degeneration in human or animal models. The contractile force generated by the smooth muscle is significantly attenuated, resulting in altered motility leading to diarrhea or constipation in IBD. The aim of this study is to clarify the altered contractility of circular and longitudinal smooth muscle layers in proximal colon of trinitrobenzen sulfonic acid (TNBS)-induced colitis mouse. Colitis was induced by direct injection of TNBS (120 mg/kg, 50% ethanol) in proximal colon of ICR mouse using a 30 G needle anesthetized with ketamin (50 mg/kg), whereas animals in the control group were injected of 50% ethanol alone. In TNBS-induced colitis, the wall of the proximal colon is diffusely thickened with loss of haustration, and showed mucosal and mucular edema with inflammatory infiltration. The colonic inflammation is significantly induced the reduction of colonic contractile activity including spontaneous contractile activity, depolarization-induced contractility, and muscarinic acetylcholine receptor-mediated contractile response in circular muscle layer compared to the longitudinal muscle layer. The inward rectification of currents, especially, important to Ca2+ and Na+ influx-induced depolarization and contraction, was markedly reduced in the TNBS-induced colitis compared to the control. The muscarinic acetylcholine-mediated contractile responses were significantly attenuated in the circular and longitudinal smooth muscle strips induced by the reduction of membrane expression of canonical transient receptor potential (TRPC) channel isoforms from the proximal colon of the TNBS-induced colitis mouse than the control.

Possible protective effect of dietary extra-virgin olive oil on experimentally induced acute colitis in adult male albino rats

“…Similar results were also described by other authors [11,23]. Increased thickness of the muscularis externa [23,24], submucosal exudate [9,20,22,24], intense cellular infiltration [17,23,24], and areas of hemorrhage [9] were findings observed in previous studies and also noticed in the present study in group II.…”

“…Several morphological changes affecting the smooth muscles in IBD were previously described by some investigators, which included bowel wall thickening with loss of haustration and folding [24]. These changes might explain the diarrhea that usually accompanies the disease.…”

Derinat Protects Skin against Ultraviolet-B (UVB)-Induced Cellular Damage

“…Incubation conditions included 10 min at 25 °C, 120 min at 37 °C, and 5 min at 85 °C. The resulting cDNAs were utilized to detect TRPC7 expression level by the quantitative PCR using SybrGreen PCR Master Mix Kit (Applied Biosystems, Carlsbad, CA, USA) and specific primers: human TRPC1 (GenBank accession number, NM_003304), forward: TAG TGA CGA GCC TCT TGA CAA and reverse: CTG GCA GTT AGA CTG GGA GA; human TRPC4 (GenBank accession number, NM_003306), forward: CTC GCT GGT ACG ATG AGT TTC and reverse: GTG GGC TTT TGG GAG CTA TCA; human TRPC6 (GenBank accession number, NM_004621), forward: GTG ATC GCT CCA CAA GCC TAT and reverse: CTG CCA ACT GTA GGG CAT TCT; human TRPC7 (GenBank accession number, NM_001167576), forward: CGA GAA ACA GCG GAA AGA CTC and reverse: TCT GGC TAA CTC GTT GCT GAG; human GAPDH (GenBank accession number, NM_ 002046), forward: TGC ACC ACC AAC TGC TTA GC and reverse: GGC ATG GAC TGT GGT CAT GAG; mouse TRPC7 (GenBank accession number, NM_012035), forward: AAC CTG ACA GCC AAT AGC ACC TTC and reverse: TGG GCC TTC AGC ACG TAT CTC; mouse GAPDH (Gene Bank accession number, NM_001001303), forward: TGT GTC CGT CGT GGA TCT GA and reverse: TTG CTG TTG AAG TCG CAG GAG [47]. Thermal cycling was employed on the Applied Biosystems 7900HT fast real-time PCR system using the following cycling conditions: 95 °C for 10 min, and 40 cycles at 95 °C for 5 s, and 60°C for 30 s. Each complete amplification stage was followed by a dissociation stage at 95 °C for 15 s and 60 °C for 30 s.…”

The TNBS-induced colitis animal model: An overview

“…That is a shared feature with the hallmark of human Crohn's disease. Moreover, mucosal edema, distortion of crypts and the formation of abscesses occur during the course of the disease [23] , [24] . Macroscopic evaluation of the colon and rectum up to 24 h after TNBS treatment revealed the presence of mucosal edema and hemorrhagic ulcerations.…”