Psychiatria Danubina · 2008
Activation of ERK and JNK MAP kinases in optic nerves of rats exposed to global cerebral ischemia.
СтатьяПоддержка исследования: вне правительства СШАНазвание 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.
Mrsić-Pelcić Jasenka, Pelcić Goran, Vitezić Dinko, Ljubicić Dulijano, Zupan Gordana, Simonić Ante
Аннотация
OBJECTIVES: To determine the influence of global cerebral ischemia on the activation of extracellular-regulated kinases (ERK) and c-Jun N-terminal kinases (JNK) in optic nerves of rats exposed to different reperfusion periods.
MATERIALS AND METHODS: Transient global cerebral ischemia (20-min duration) was induced by the four-vessel occlusion method. After different reperfusion periods (5 and 10 min; 1; 6 and 12 h after ischemia), optic nerves were extracted and ERK and JNK activation signals were determined by Western immunoblot analyses.
RESULTS: The activation signals of ERK and JNK were detected within first 10 min of reperfusion, but striking activation for both enzymes was found 1 h after ischemia. After a transient decrease, the activation of ERK returned to peak level after 12 h of reperfusion in the second wave of kinase activation. In that period, a slight increase of JNK activation was registered.
CONCLUSION: Our results demonstrated for the first time that ERK and JNK were activated in rat optic nerves during early and later periods of reperfusion, suggesting their potential active role in the response of cerebral white matter tissue to ischemic injury.
MATERIALS AND METHODS: Transient global cerebral ischemia (20-min duration) was induced by the four-vessel occlusion method. After different reperfusion periods (5 and 10 min; 1; 6 and 12 h after ischemia), optic nerves were extracted and ERK and JNK activation signals were determined by Western immunoblot analyses.
RESULTS: The activation signals of ERK and JNK were detected within first 10 min of reperfusion, but striking activation for both enzymes was found 1 h after ischemia. After a transient decrease, the activation of ERK returned to peak level after 12 h of reperfusion in the second wave of kinase activation. In that period, a slight increase of JNK activation was registered.
CONCLUSION: Our results demonstrated for the first time that ERK and JNK were activated in rat optic nerves during early and later periods of reperfusion, suggesting their potential active role in the response of cerebral white matter tissue to ischemic injury.