丹参乙酸镁减轻脑缺血/再灌注诱导的神经细胞凋亡作用及机制

目的 探讨丹参乙酸镁对于大鼠脑缺血/再灌注损伤中的保护作用及其机制。方法动物实验采用大鼠线栓法缺血/再灌注模型,使大鼠脑缺血2 h后,再灌注24 h。细胞实验采用NG108-15神经细胞株缺氧/复氧模型,低氧无糖培养2 h后,复氧24 h。检测神经细胞凋亡、NADPH氧化酶 (NOX)活性及H₂O₂水平。结果与模型组比较,丹参乙酸镁组大鼠脑组织神经细胞凋亡明显下降,NOX活性和H₂O₂水平均降低。结论丹参乙酸镁具有抗脑缺血/再灌注损伤的作用,其机制与抑制NOX活性,减少H₂O₂生成有关。

Effect of magnesium lithospermate B on cerebral ischemia/reperfusion- induced apoptosis and the underlying mechanisms

Objective To investigate whether lithospermate B is able to protect the rat brain from ischemia/reperfusion injury and the underlying mechanism.MethodRats were subjected to 2 h of cerebral ischemia and 24 h of reperfusion to establish anischemia/reperfusion injury model.In a NG108-15 nerve cell hypoxia/reoxygenation (H/R) injury model,cells were cultured in 2 h of hypoxia and 24 h of reoxygenation.And cellular apoptosis,nicotinamide adenine dinucleotide phosphate-oxidase (NOX)activity,and H₂O₂ content were examined.ResultAdministration of salvia magnesium lithospermate B reduced apoptosis of nerve cells with a decrease in nicotinamide adenine dinucleotide phosphate-oxidase activity and H₂O₂ production in the rat brains,compared with model group.In the experiments,the number of iHoechst staining positive cells,nicotinamide adenine dinucleotide phosphate-oxidase activity and H₂O₂ level were decreased by the intervention of drugs.ConclusionThe results suggest that lithospermate B is able to protect the brain from ischemia/reperfusion oxidative injury,which is related to the inhibition of nicotinamide adenine dinucleotide phosphate-oxidase and a reduction of reactive oxygen species production.