摘要
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H_2O_2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H_2O_2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H_2O_2生成有关。
Objective To investigate whether lithospermate B is able to protect the rat brain from ischemia/reperfusion injury and the underlying mechanism. Method Rats 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 H_2O_2 content were examined. Result Administration of salvia magnesium lithospermate B reduced apoptosis of nerve cells with a decrease in nicotinamide adenine dinucleotide phosphate-oxidase activity and H_2O_2 production in the rat brains,compared with model group.In the experiments,the number of i Hoechst staining positive cells,nicotinamide adenine dinucleotide phosphate-oxidase activity and H_2O_2 level were decreased by the intervention of drugs. Conclusion The 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.
出处
《中南医学科学杂志》
CAS
2017年第5期465-470,共6页
Medical Science Journal of Central South China
基金
湖南省教育厅一般项目(15C0161)药学类专业校企合作人才培养示范基地(湘教通[2014]272号)
关键词
丹参乙酸镁
缺血/再灌注
氧化应激
magnesium lithospermate B
ischemia/reperfusion injury
oxidative stress
