Aquaporin 3 and 8 are down-regulated in TNBS-induced rat colitis

• Published in: Biochemical and biophysical research communications 2014-01, Vol.443 (1), p.161-166
• Main Authors: Zhao, Guangxi, Li, Jing, Wang, Jiyao, Shen, Xizhong, Sun, Jianyong
• Format: Article
• Language: English
• Subjects: 2,4,6-Trinitrobenzene sulfonic acid; Animals; AQP3; AQP8; Aquaporin 3 - metabolism; Aquaporins - metabolism; Colitis; Colon - drug effects; Colon - metabolism; Crohn Disease - chemically induced; Crohn Disease - metabolism; Crohn Disease - pathology; Disease Models, Animal; Down-Regulation; Female; Rat; Rats; Rats, Sprague-Dawley; Trinitrobenzenesulfonic Acid - pharmacology
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2013.11.067

•AQP3 and AQP8 were down-regulated in TNBS-induced rat colitis.•There was no shift in localization of AQP3 and AQP8 in TNBS-induced rat colitis.•The vicious circle of inflammatory mediators-AQPs-inflammation was speculated. Aquaporins (AQPs) plays an important role in transcellular water movement, but the AQPs expression profile has not been demonstrated in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis which closely mimics human Crohn’s disease (CD) histopathologically. To solve the problem, 30 female Sprague–Dawley (SD) rats were randomly divided into a model group (n=18), an ethanol control group (n=6) and a normal control group (n=6). On day 1, the rats in the model group received TNBS+50% ethanol via the rectum, while the ethanol control rats received an equal volume of 50% ethanol and the normal control rats did not receive any treatment. All rats were sacrificed on day 7, and ileum, proximal colon and distal colon specimens were obtained to examine the alteration in AQP3 and AQP8 using real-time polymerase chain reaction, Western blot analysis and immunohistochemistry. As a result, exposure to TNBS+ethanol resulted in a marked decrease in both the mRNA and protein expression of AQP3 and AQP8, with the exception of AQP8 protein which was negative in the distal colon in all three groups. These reductions in AQP3 and AQP8 were accompanied by an increase in intestinal inflammation and injury. The results obtained here implied that both AQP3 and AQP8 may be involved in the pathogenesis of inflammatory bowel disease.