氧化应激促进了脑缺血/再灌注损伤。本项目预实验首次发现牡荆素B1能显著减轻大鼠脑缺血/再灌注（IR）损伤，抑制NADPH氧化酶2 (NOX2)和NOX4表达, 升高miR-92b水平。基于上述结果，我们率先从以下方面探讨牡荆素B1抗脑缺血/再灌注氧化损伤的作用及机制：① 建立大鼠脑IR模型，结合药物干预、NOX RNA干扰或miR-92b等 agomir干预，检测脑梗死体积、NOX2、NOX4表达等指标，初步确定牡荆素B1抗脑缺血/再灌注损伤作用及机制；② 建立神经细胞低氧/复氧损伤模型，结合药物干预、NOX基因沉默、miR-92b等 mimics干预及荧光素报告基因技术，检测上述相关指标, 阐明牡荆素B1神经保作用及机制。该研究将为脑缺血/再灌注氧化损伤的防治提供新的理论依据。

Oxidative stress promotes the progress of cerebral ischemia/reperfusion injury.This study first found that vetexin B1 can significantly protect rats from cerebral ischemia/reperfusion injury through inhibiting NADPH oxidase 2(NOX2) and NOX4 and increasing miR-92b level. Base on the above results, we first probe into the role in against cerebral ischemia/reperfusion injury and its underlying mechanism from the following aspects:1)to construct the cerebral ischemia/reperfusion model in rats and combination with drugs intervention, NOX RNA interference, miR-92b and other miRNAs agomirs intervention, and measure the brain infarct volume and the expression of NOX2 or NOX4 or others to preliminarily determine the effects of vitexin B1 on against cerebral ischemia/reperfusion injury and its underlying mechanism;2)To construct the hypoxia/reoxygenation model in neuron cells and combination with NOX gene silencing ,miR-92b and other miRNAs mimics intervention and Luciferase reporter gene technology, and measure the related indices to illustrate the neuroprotection effects of vitexin B1 and its underlying mechanism.This study will provide new theoretical basis for cerebral ischemia/reperfusion oxidative damage prevention and treatment.