Der Orthopade · 2005
[In vitro effects of diclofenac and selective cyclooxygenase-2 inhibitors on prostaglandin release from inflamed bursa subacromialis tissue in patients with subacromial syndrome].
Клиническое исследованиеАннотация на английскомСтатьяНазвание 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.
Knorth H, Wittenberg R H, Dorfmüller P, Lebert R, Schmidt W E, Peskar B M, Wiese M, Heukamp M, Willburger R E
Аннотация
BACKGROUND: To compare the in vitro effects of selective COX-2 inhibitors (L-745,337, NS-398 and DFU) and of COX-unspecific diclofenac on release of PGE(2 )and 6-keto-PGF(1alpha) from inflamed bursa subacromialis tissue (IBST) obtained from a total of 35 patients with shoulder impingement syndrome (SIS).
PATIENTS AND METHODS: Bursal specimens were incubated in the presence of drugs (0.01-1000 microM) for 20 min and 16 h.
RESULTS: After 20 min 10 microM diclofenac significantly inhibited formation of PGE(2) and 6-keto-PGF(1alpha), whereas L-745,337 and NS-398 (10-1000 microM) induced significant inhibition only at concentrations > or =100 microM. In contrast to equimolar diclofenac, DFU (0.01-10 microM) induced no inhibition of bursal PGE(2) release but a dose-dependent, although statistically not significant inhibition after 16 h. The inhibitory potency of diclofenac (0.01-10 microM) was even more increased during long-term incubation showing greater inhibition than DFU at all concentrations studied.
CONCLUSION: The data suggest that in IBST in SIS in vitro the majority of PG is generated via the COX-1 pathway.
PATIENTS AND METHODS: Bursal specimens were incubated in the presence of drugs (0.01-1000 microM) for 20 min and 16 h.
RESULTS: After 20 min 10 microM diclofenac significantly inhibited formation of PGE(2) and 6-keto-PGF(1alpha), whereas L-745,337 and NS-398 (10-1000 microM) induced significant inhibition only at concentrations > or =100 microM. In contrast to equimolar diclofenac, DFU (0.01-10 microM) induced no inhibition of bursal PGE(2) release but a dose-dependent, although statistically not significant inhibition after 16 h. The inhibitory potency of diclofenac (0.01-10 microM) was even more increased during long-term incubation showing greater inhibition than DFU at all concentrations studied.
CONCLUSION: The data suggest that in IBST in SIS in vitro the majority of PG is generated via the COX-1 pathway.