Peptides · 2023
Irisin alleviates hyperoxia-induced bronchopulmonary dysplasia through activation of Nrf2/HO-1 pathway.
СтатьяПоддержка исследования: вне правительства СШАНазвание 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.
Zhao Zi-Wen, Lin Xiao-Xia, Guo Yong-Zhe, He Xi, Zhang Xin-Tao, Huang Yu
Аннотация
BACKGROUND: Bronchopulmonary dysplasia (BPD) is a common pulmonary injury among premature infants, which is often caused by hyperoxia exposure. Irisin is a novel hormone-like myokine derived mainly from skeletal muscles as well as adipose tissues. Many studies have indicated that Irisin exert a variety of properties against hyperoxia-induced inflammation and oxidative stress (OS). We aimed to evaluate the effects of irisin on hyperoxia-induced lung injury explore the underlying mechanisms.
METHODS: BPD model was established after exposing newborn mouse to 85% oxygen. BPD mouse received continuous intraperitoneal injection of irisin at a dose of 25 μg/kg/day. Lung tissues were collected for histological examination at 7 and 14 days after birth. The alveolarization and alveolar vascularization of each animal was assessed. Levels of oxidative stress indicators, and the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in lung tissues were detected at 14 days after birth.
RESULTS: Hyperoxia exposure induced a markedly alveolar simplification and a disrupted alveolar angiogenesis, which was ameliorated by irisin treatment. The hyperoxia-induced increase in these oxidative stress indicators was significantly reversed by irisin treatment. The Nrf2/HO-1 pathway is inducted in the hyperoxia-induced BPD mouse model, which is further activated by irisin treatment.
CONCLUSION: Our results demonstrated the beneficial effects of irisin in reducing the OS, enhancing alveolarization, and promoting vascular development through activation of Nrf2/HO-1 axis in a hyperoxia-induced experimental model of BPD.
METHODS: BPD model was established after exposing newborn mouse to 85% oxygen. BPD mouse received continuous intraperitoneal injection of irisin at a dose of 25 μg/kg/day. Lung tissues were collected for histological examination at 7 and 14 days after birth. The alveolarization and alveolar vascularization of each animal was assessed. Levels of oxidative stress indicators, and the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in lung tissues were detected at 14 days after birth.
RESULTS: Hyperoxia exposure induced a markedly alveolar simplification and a disrupted alveolar angiogenesis, which was ameliorated by irisin treatment. The hyperoxia-induced increase in these oxidative stress indicators was significantly reversed by irisin treatment. The Nrf2/HO-1 pathway is inducted in the hyperoxia-induced BPD mouse model, which is further activated by irisin treatment.
CONCLUSION: Our results demonstrated the beneficial effects of irisin in reducing the OS, enhancing alveolarization, and promoting vascular development through activation of Nrf2/HO-1 axis in a hyperoxia-induced experimental model of BPD.