The International journal of neuroscience · 2017
Annexin A10 contributes to chronic constrictive injury-induced pain through activating ERK1/2 signalling in rats.
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.
Li Feng, Xue Zhou-Ya, Liu Xiang, Bai Gang, Wang Yuan-Lin
Аннотация
PURPOSE: The current study aims at investigating the downstream targets of spinal Annexin A10 in modulating neuropathic pain.
MATERIALS AND METHODS: Paw withdrawal latency and paw withdrawal threshold were measured to evaluate the pain-associated behaviour in rats. The expression of spinal Annexin A10, phosphorylated-extracellular regulated kinase 1/2 and extracellular regulated kinase were detected by western blotting. The level of tumour necrosis factor-α and interleukine-1β was tested by enzyme-linked immunosorbent assay (ELISA) kits.
RESULTS: Chronic constrictive injury caused pain hypersensitivity in rats, along with increased expression of spinal Annexin A10, phosphorylated-extracellular regulated kinase 1/2, tumour necrosis factor-α and interleukine-1β in rats. Knockdown of spinal Annexin A10 suppressed the chronic constrictive injury-induced hyperalgesia, and inhibited the chronic constrictive injury-induced increased expression of phosphorylated-extracellular regulated kinase 1/2, tumour necrosis factor-α and interleukine-1β in the spinal cord. Inhibition of spinal extracellular regulated kinase activation decreased the release of tumour necrosis factor-α and interleukine-1β, but did not change the increased expression of Annexin A10 caused by chronic constrictive injury.
CONCLUSIONS: Annexin A10 contributed to the development of neuropathic pain by activating spinal extracellular regulated kinase signalling and the subsequent release of tumour necrosis factor-α and interleukine-1β in the spinal cord.
MATERIALS AND METHODS: Paw withdrawal latency and paw withdrawal threshold were measured to evaluate the pain-associated behaviour in rats. The expression of spinal Annexin A10, phosphorylated-extracellular regulated kinase 1/2 and extracellular regulated kinase were detected by western blotting. The level of tumour necrosis factor-α and interleukine-1β was tested by enzyme-linked immunosorbent assay (ELISA) kits.
RESULTS: Chronic constrictive injury caused pain hypersensitivity in rats, along with increased expression of spinal Annexin A10, phosphorylated-extracellular regulated kinase 1/2, tumour necrosis factor-α and interleukine-1β in rats. Knockdown of spinal Annexin A10 suppressed the chronic constrictive injury-induced hyperalgesia, and inhibited the chronic constrictive injury-induced increased expression of phosphorylated-extracellular regulated kinase 1/2, tumour necrosis factor-α and interleukine-1β in the spinal cord. Inhibition of spinal extracellular regulated kinase activation decreased the release of tumour necrosis factor-α and interleukine-1β, but did not change the increased expression of Annexin A10 caused by chronic constrictive injury.
CONCLUSIONS: Annexin A10 contributed to the development of neuropathic pain by activating spinal extracellular regulated kinase signalling and the subsequent release of tumour necrosis factor-α and interleukine-1β in the spinal cord.