Abstract
Apigenin is a natural flavonoid found in several dietary plant foods as vegetables and fruits. To investigate potential anti-ischemia/reperfusion injury properties of apigenin in vitro, cell proliferation assay, tube formation, cell migration, apoptosis, and autophagy were performed in human brain microvascular endothelial cells (HBMVECs) after oxygen-glucose deprivation/reoxygenation (OGD/R). The effect of apigenin was also explored in rats after middle cerebral artery occlusion/reperfusion (MCAO/R) via neurobehavioral scores, pathological examination, and measurement of markers involved in ischemia/reperfusion injury. Data in vitro indicated that apigenin could prompt cell proliferation, tube formation, and cell migration while inhibiting apoptosis and autophagy by affecting Caveolin-1/VEGF, Bcl-2, Caspase-3, Beclin-1, and mTOR expression. Results in vivo showed that apigenin significantly reduced neurobehavioral scores and volume of cerebral infarction while prompting vascular endothelial cell proliferation by upregulating VEGFR2/CD34 double-labeling endothelial progenitor cell (EPC) number and affecting Caveolin-1, VEGF, and eNOS expression in brain tissue of MCAO/R rats. All the data suggested that apigenin may be protective for the brain against ischemia/reperfusion injury by alleviating apoptosis and autophagy, promoting cell proliferation in HBMVECs of OGD/R, and attenuating brain damage and improved neurological function in rats of MCAO/R through the Caveolin-1/VEGF pathway.
Highlights
Ischemia such as stroke, myocardial infarction, and peripheral vascular disease is one of the most common causes of disability and death worldwide [1]
We have demonstrated that Caveolin-1 decreased cerebral infarct volume, facilitated angiogenesis and neurogenesis, and promoted neurological recovery by upregulating the Caveolin-1/vascular endothelial growth factor (VEGF) signaling pathway in a rat model of middle cerebral artery occlusion (MCAO) in our previous study [15,16,17]
Based on our previous study, we explored the effect of apigenin on the Caveolin-1/VEGF signaling pathway in an oxygen-glucose deprivation/reoxygenation (OGD/R) model of human brain microvascular endothelial cells (HBMVECs) and MCAO rat model
Summary
Myocardial infarction, and peripheral vascular disease is one of the most common causes of disability and death worldwide [1]. Apigenin pretreatment can protect against renal ischemia/reperfusion via the activation of the JAK2/STAT3 signaling pathway [7]. VEGF (vascular endothelial growth factor) associates with angiogenesis protecting neurons from ischemic insults and promoting neurogenesis after cerebral ischemic injury [11,12,13,14]. We have demonstrated that Caveolin-1 decreased cerebral infarct volume, facilitated angiogenesis and neurogenesis, and promoted neurological recovery by upregulating the Caveolin-1/VEGF signaling pathway in a rat model of middle cerebral artery occlusion (MCAO) in our previous study [15,16,17]. Based on our previous study, we explored the effect of apigenin on the Caveolin-1/VEGF signaling pathway in an oxygen-glucose deprivation/reoxygenation (OGD/R) model of human brain microvascular endothelial cells (HBMVECs) and MCAO rat model
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