Alimentary pharmacology & therapeutics · 2001
Up-regulation of cyclooxygenase-1 and -2 in human gastric ulcer.
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.
To K F, Chan F K, Cheng A S, Lee T L, Ng Y P, Sung J J
Аннотация
BACKGROUND: The expression of cyclooxygenase (COX) in human gastric ulcers is unknown.
AIM: To study the expression and cellular localization of cyclooxygenase in human gastric ulcers.
METHODS: A total of 38 surgical gastric ulcer specimens were studied; 20 were Helicobacter pylori-positive and 18 were associated with NSAID use. Twenty non-ulcerated, histologically normal gastric specimens were used as controls. The cellular localization of COX-1 and COX-2 were determined by immunohistochemistry and double immunofluorescence. Cyclooxygenase messenger RNA (mRNA) was measured by reverse transcription-polymerase chain reaction and localized by in situ hybridization.
RESULTS: In control specimens, COX-1 was detected in stromal cells in the lamina propria. There was focal and weak immunostaining for COX-2 in the foveolar epithelium. At the ulcer edge, COX-1 was significantly increased in lamina propria cells whereas COX-2 was strongly expressed in the hyperplastic foveolar epithelium in H. pylori- and non-steroidal anti-inflammatory drugs (NSAID)-associated ulcers. At the ulcer base, there was strong expression of COX-1 and COX-2 in myofibroblasts, macrophages and endothelial cells in the granulation tissue, irrespective of H. pylori status or NSAID use. Messenger RNA of COX-1 and COX-2 were demonstrated by reverse transcription-polymerase chain reaction. Double immunofluorescence and in situ hybridization confirmed the cellular localization of cyclooxygenase at protein and mRNA levels, respectively.
CONCLUSION: Both COX-1 and COX-2 are up-regulated in human gastric ulcers.
AIM: To study the expression and cellular localization of cyclooxygenase in human gastric ulcers.
METHODS: A total of 38 surgical gastric ulcer specimens were studied; 20 were Helicobacter pylori-positive and 18 were associated with NSAID use. Twenty non-ulcerated, histologically normal gastric specimens were used as controls. The cellular localization of COX-1 and COX-2 were determined by immunohistochemistry and double immunofluorescence. Cyclooxygenase messenger RNA (mRNA) was measured by reverse transcription-polymerase chain reaction and localized by in situ hybridization.
RESULTS: In control specimens, COX-1 was detected in stromal cells in the lamina propria. There was focal and weak immunostaining for COX-2 in the foveolar epithelium. At the ulcer edge, COX-1 was significantly increased in lamina propria cells whereas COX-2 was strongly expressed in the hyperplastic foveolar epithelium in H. pylori- and non-steroidal anti-inflammatory drugs (NSAID)-associated ulcers. At the ulcer base, there was strong expression of COX-1 and COX-2 in myofibroblasts, macrophages and endothelial cells in the granulation tissue, irrespective of H. pylori status or NSAID use. Messenger RNA of COX-1 and COX-2 were demonstrated by reverse transcription-polymerase chain reaction. Double immunofluorescence and in situ hybridization confirmed the cellular localization of cyclooxygenase at protein and mRNA levels, respectively.
CONCLUSION: Both COX-1 and COX-2 are up-regulated in human gastric ulcers.