Clinical hemorheology and microcirculation · 2024
Adipokine vaspin maintains angiogenesis and neurological function during cerebral ischemia-reperfusion via suppressing endoplasmic reticulum stress.
СтатьяНазвание 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.
Yan Wentao, He Xiuhua, Wang Guanjun, Hu Guochao, Cui Bin
Аннотация
INTRODUCTION: Visceral adipose tissue-derived serine protease inhibitor (vaspin) is an adipokine. It has been reported that decreased serum vaspin levels are significantly associated with stroke severity and prognosis.
OBJECTIVE: This article aims to explore the theoretical feasibility of vaspin supplementation for cerebral ischemia-reperfusion (I/R) injury.
METHODS: The I/R mouse models were constructed by the middle cerebral artery occlusion (MCAO) method, and the effects of vaspin on cerebral infarction, neurological function, angiogenesis and endoplasmic reticulum (ER) stress were explored. To verify the mediation of ER stress in the regulation of vaspin, human brain microvascular endothelial cells (HBMECs) were subjected to ER stress agonist tunicamycin in vitro. The impacts of vaspin and tunicamycin on oxygen glucose deprivation/ recovery (OGD/R)-induced cell viability, apoptosis, and angiogenesis were examined.
RESULTS: Vaspin inhibited blood-brain barrier breakdown and infarction occurred in the brain tissue of the I/R mice. Vaspin also enhanced cerebral neovascularization and reduced the apoptosis. Additional tunicamycin increased the apoptosis of HBMECs and inhibited angiogenesis, reversing the protective effect of vaspin on cells.
CONCLUSION: Together, this study reveals that vaspin supplementation reduces cerebral infarction and works against neurological dysfunction. It maintains the survival and angiogenesis capacity of HBMECs by inhibiting ER stress.
OBJECTIVE: This article aims to explore the theoretical feasibility of vaspin supplementation for cerebral ischemia-reperfusion (I/R) injury.
METHODS: The I/R mouse models were constructed by the middle cerebral artery occlusion (MCAO) method, and the effects of vaspin on cerebral infarction, neurological function, angiogenesis and endoplasmic reticulum (ER) stress were explored. To verify the mediation of ER stress in the regulation of vaspin, human brain microvascular endothelial cells (HBMECs) were subjected to ER stress agonist tunicamycin in vitro. The impacts of vaspin and tunicamycin on oxygen glucose deprivation/ recovery (OGD/R)-induced cell viability, apoptosis, and angiogenesis were examined.
RESULTS: Vaspin inhibited blood-brain barrier breakdown and infarction occurred in the brain tissue of the I/R mice. Vaspin also enhanced cerebral neovascularization and reduced the apoptosis. Additional tunicamycin increased the apoptosis of HBMECs and inhibited angiogenesis, reversing the protective effect of vaspin on cells.
CONCLUSION: Together, this study reveals that vaspin supplementation reduces cerebral infarction and works against neurological dysfunction. It maintains the survival and angiogenesis capacity of HBMECs by inhibiting ER stress.