Histology and histopathology · 2024
Prevention of colon enlargement by TNF-α antagonist in a streptozotocin-induced diabetic rat model.
СтатьяНазвание и аннотация: Перевод в очереди
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.
Sholikah Tri Agusti, Septyaningtrias Dian Eurike, Sumiwi Yustina Andwi Ari, Muthmainah Muthmainah, Susilowati Rina
Аннотация
PURPOSE: We investigated the effect of tumor necrosis factor (TNF)-α antagonist on the structure and function of the streptozotocin-nicotinamide (STZ-NA)-induced diabetic rat colon.
METHODS: Thirty rats were divided into normal control (NC), diabetic control (DC), and diabetic etanercept (DE) groups. The DE group was injected with etanercept twice a week. Blood glucose, body weight, fecal pellet, colonic transit time, and plasma TNF-α were measured. The colon was dissected out, followed by weight and length measurements. Toluidine blue and Verhoeff's staining, immunohistochemistry for TNF-α, RAGE, iNOS, arginase, and western blot for RAGE were performed on the colonic tissue.
RESULTS: Administration of TNF-α antagonist had no significant effect on the body weight and blood glucose level of the diabetic groups. However, the DE group had a shorter and lighter colon and less coarse and less dense collagen fibers in the submucosal layer than the DC group. Weaker immunoreactivity of TNF-α, RAGE, iNOS, and arginase I was observed in colon tissue sections of the DE groups compared with the DC group. Although the etanercept effect on colonic function was not significantly different, the preventive effect size of etanercept on colon remodeling was considerably large, as shown by calculated-Cohen's d>0.8.
CONCLUSIONS: TNF-α signaling in the colonic tissue of diabetic rats has a strong effect on tissue remodeling, leading to colon enlargement. TNF-α antagonists may be beneficial in preventing diabetic-related pathology in the colon in combination with anti-diabetic drugs.
METHODS: Thirty rats were divided into normal control (NC), diabetic control (DC), and diabetic etanercept (DE) groups. The DE group was injected with etanercept twice a week. Blood glucose, body weight, fecal pellet, colonic transit time, and plasma TNF-α were measured. The colon was dissected out, followed by weight and length measurements. Toluidine blue and Verhoeff's staining, immunohistochemistry for TNF-α, RAGE, iNOS, arginase, and western blot for RAGE were performed on the colonic tissue.
RESULTS: Administration of TNF-α antagonist had no significant effect on the body weight and blood glucose level of the diabetic groups. However, the DE group had a shorter and lighter colon and less coarse and less dense collagen fibers in the submucosal layer than the DC group. Weaker immunoreactivity of TNF-α, RAGE, iNOS, and arginase I was observed in colon tissue sections of the DE groups compared with the DC group. Although the etanercept effect on colonic function was not significantly different, the preventive effect size of etanercept on colon remodeling was considerably large, as shown by calculated-Cohen's d>0.8.
CONCLUSIONS: TNF-α signaling in the colonic tissue of diabetic rats has a strong effect on tissue remodeling, leading to colon enlargement. TNF-α antagonists may be beneficial in preventing diabetic-related pathology in the colon in combination with anti-diabetic drugs.