Neuroreport · 2021
Dendrobium nobile Lindl. polysaccharides reduce cerebral ischemia/reperfusion injury in mice by increasing myeloid cell leukemia 1 via the downregulation of miR-134.
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.
Liu Jing, Han Yu, Zhu Tao, Yang Qing, Wang Heming, Zhang Hao
Аннотация
OBJECTIVE: The traditional Chinese medicine, Dendrobium nobile Lindl. polysaccharides (DNLP), reportedly has neuroprotective effects. However, its effects following ischemic stroke remain unclear. This study aimed to explore the role and mechanism of DNLP in experimental models of inflammation and apoptosis.
METHODS: Inflammation and apoptosis were induced by in vivo ischemia/reperfusion and by in vitro oxygen glucose deprivation/reperfusion (OGD/R). In the in vivo model, immediately after the induction of cerebral ischemia, 50, 100, and 200 mg/kg DNLP were injected intraperitoneally. We subsequently detected indicators of neuronal damage.
RESULTS: Treatment with Dendrobium nobile Lindl. polysaccharide significantly reduced cerebral ischemic injury. After in vivo and in vitro middle cerebral artery occlusion/reperfusion or OGD/R-induced hypoxia injury, miR-134 expression in neurons was significantly increased. Altering the expression of miR-134 induced changes in myeloid cell leukemia 1 (MCL-1), one of its target proteins. In addition, DNLP significantly downregulated the in vivo and in vitro expression of miR-134 after ischemic injury, and influenced inflammation and apoptotic proteins by altering the level of MCL-1 protein. DNLP also had a protective effect on neurons damaged by OGD/R, which could improve cell survival rates and inhibit lactate dehydrogenase release as well as apoptosis.
CONCLUSIONS: DNLP may protect the brain and neurons from hypoxic damage in mice with ischemic stroke by activating MCL-1 and downregulating miR-134, providing a new therapeutic target for ischemic stroke.
METHODS: Inflammation and apoptosis were induced by in vivo ischemia/reperfusion and by in vitro oxygen glucose deprivation/reperfusion (OGD/R). In the in vivo model, immediately after the induction of cerebral ischemia, 50, 100, and 200 mg/kg DNLP were injected intraperitoneally. We subsequently detected indicators of neuronal damage.
RESULTS: Treatment with Dendrobium nobile Lindl. polysaccharide significantly reduced cerebral ischemic injury. After in vivo and in vitro middle cerebral artery occlusion/reperfusion or OGD/R-induced hypoxia injury, miR-134 expression in neurons was significantly increased. Altering the expression of miR-134 induced changes in myeloid cell leukemia 1 (MCL-1), one of its target proteins. In addition, DNLP significantly downregulated the in vivo and in vitro expression of miR-134 after ischemic injury, and influenced inflammation and apoptotic proteins by altering the level of MCL-1 protein. DNLP also had a protective effect on neurons damaged by OGD/R, which could improve cell survival rates and inhibit lactate dehydrogenase release as well as apoptosis.
CONCLUSIONS: DNLP may protect the brain and neurons from hypoxic damage in mice with ischemic stroke by activating MCL-1 and downregulating miR-134, providing a new therapeutic target for ischemic stroke.