Digestion · 2007
Effect of passive cigarette smoking on colonic alpha7-nicotinic acetylcholine receptors in TNBS-induced colitis in rats.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Sun Ya P, Wang Hua H, He Qun, Cho Chi H
Аннотация
BACKGROUND AND AIMS: Cigarette smoking affects colonic inflammation, but the exact mechanism by which it does so is unclear. The aim of this study was to investigate the underlying mechanism by examining the effect of cigarette smoking on 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats.
METHOD: Experimental colitis was induced by administrating TNBS enema in Sprague-Dawley rats. The effect of cigarette smoking was assessed by measuring the colonic edema, mucosal lesion area, histopathological score, mucosal myeloperoxidase (MPO) activity and tumor necrosis factor-alpha (TNF-alpha). The expression of alpha7-nicotinic acetylcholine receptor (alpha7nAChR) was examined after cigarette smoking to identify whether the alpha7nAChR is involved in inflammation.
RESULTS: TNBS induced severe colitis as evidenced by increased colonic edema, mucosal lesion area, histopathological score, MPO activity, and TNF-alpha level. Inflammation was aggravated by cigarette smoke exposure. Colonic tissue expressed alpha7nAChR (0.41 +/- 0.11), and TNBS up-regulated the receptor expression (0.46 +/- 0.11), but the difference was not significant (p > 0.05). Cigarette smoking with 2 and 4% respectively significantly increased the expression of alpha7nAChR (0.55 +/- 0.05 and 0.64 +/- 0.08) (p < 0.05).
CONCLUSIONS: The up-regulated expression of alpha7nAChR after exposure to cigarette smoking indicates that alpha7nAChR in colonic tissue may be involved in cigarette smoking damage in TNBS-induced colitis in rats.
METHOD: Experimental colitis was induced by administrating TNBS enema in Sprague-Dawley rats. The effect of cigarette smoking was assessed by measuring the colonic edema, mucosal lesion area, histopathological score, mucosal myeloperoxidase (MPO) activity and tumor necrosis factor-alpha (TNF-alpha). The expression of alpha7-nicotinic acetylcholine receptor (alpha7nAChR) was examined after cigarette smoking to identify whether the alpha7nAChR is involved in inflammation.
RESULTS: TNBS induced severe colitis as evidenced by increased colonic edema, mucosal lesion area, histopathological score, MPO activity, and TNF-alpha level. Inflammation was aggravated by cigarette smoke exposure. Colonic tissue expressed alpha7nAChR (0.41 +/- 0.11), and TNBS up-regulated the receptor expression (0.46 +/- 0.11), but the difference was not significant (p > 0.05). Cigarette smoking with 2 and 4% respectively significantly increased the expression of alpha7nAChR (0.55 +/- 0.05 and 0.64 +/- 0.08) (p < 0.05).
CONCLUSIONS: The up-regulated expression of alpha7nAChR after exposure to cigarette smoking indicates that alpha7nAChR in colonic tissue may be involved in cigarette smoking damage in TNBS-induced colitis in rats.