Antioxidant Effect of Salvianolic Acid B on Hippocampal CA1Neurons in Mice with Cerebral Ischemia and Reperfusion Injury  

作　　者：蒋玉凤 刘智勤 崔巍 张文通 龚家培 王玺玫 张颖 杨美娟 

机构地区：[1]Department of Pathology,Beijing University of Chinese Medicine [2]Department of Pharmacology,College of Pharmacy,Hebei University [3]Beijing Institute of Heart,Lung and Vessel Diseases,Beijing Anzhen Hospital,Capital University of Medical Sciences [4]Department of Province Neurology,Beijing Huimin Hospital

出　　处：《Chinese Journal of Integrative Medicine》2015年第7期516-522,共7页中国结合医学杂志（英文版）

基　　金：Supported by the National Natural Science Foundation of China(No.30472281)

摘　　要：Objetive： TO investigate the neuroprotective effects and underlying mechanisms of salvianolic acid B （Sal B） extracted from Salvia miltiorrhiza on hippocampal CA1 neurons in mice with cerebral ischemia reperfusion injury. Methods： Forty male National Institute of Health （NIH） mice were randomly divided into 4 groups with 10 animals each, including the sham group, the model group, the SalB group （SalB 22.5 mg/kg） and the nimodipine （Nim） group （Nim 1 mg/kg）. A mouse model of cerebral ischemia and reperfusion injury was established by bilateral carotid artery occlusion for 30 rain followed by 24-h reperfusion. The malondialdehyde （MDA） content, the nitric oxide synthase （NOS） activity, the superoxide dismutase （SOD） activity and total anti- oxidant capability （T-AOC） of the pallium were determined by biochemistry methods. The morphologic changes and Bcl-2 and Bax protein expression in hippocampal CA1 neurons were observed by using hematoxylin- eosin staining and immunohistochemistry staining, respectively. Results： In the SalB group, the MDA content and the NOS activity of the pallium in cerebral ischemia-reperfusion mice significantly decreased and the SOD activity and the T-AOC significantly increased, as compared with the model group （P〈0.05 or P〈0.01）. The SalB treatment also rescued neuronal loss （P〈0.01） in the hippocampal CA1 region, strongly promoted Bcl-2 protein expression （P〈0.01） and inhibited Bax protein expression （P〈0.05）. Conclusions： SalB increases the level of antioxidant substances and decreases free radicals production. Moreover, it also improves Bcl-2 expression and reduces Bax expression. SalB may exert the neuroprotective effect through mitochondria-dependent pathway on hippocampal CA1 neurons in mice with cerebral ischemia and reperfusion injury and suggested that SalB represents a promising candidate for the prevention and treatment of ischemic cerebrovascular disease.Objetive： TO investigate the neuroprotective effects and underlying mechanisms of salvianolic acid B （Sal B） extracted from Salvia miltiorrhiza on hippocampal CA1 neurons in mice with cerebral ischemia reperfusion injury. Methods： Forty male National Institute of Health （NIH） mice were randomly divided into 4 groups with 10 animals each, including the sham group, the model group, the SalB group （SalB 22.5 mg/kg） and the nimodipine （Nim） group （Nim 1 mg/kg）. A mouse model of cerebral ischemia and reperfusion injury was established by bilateral carotid artery occlusion for 30 rain followed by 24-h reperfusion. The malondialdehyde （MDA） content, the nitric oxide synthase （NOS） activity, the superoxide dismutase （SOD） activity and total anti- oxidant capability （T-AOC） of the pallium were determined by biochemistry methods. The morphologic changes and Bcl-2 and Bax protein expression in hippocampal CA1 neurons were observed by using hematoxylin- eosin staining and immunohistochemistry staining, respectively. Results： In the SalB group, the MDA content and the NOS activity of the pallium in cerebral ischemia-reperfusion mice significantly decreased and the SOD activity and the T-AOC significantly increased, as compared with the model group （P〈0.05 or P〈0.01）. The SalB treatment also rescued neuronal loss （P〈0.01） in the hippocampal CA1 region, strongly promoted Bcl-2 protein expression （P〈0.01） and inhibited Bax protein expression （P〈0.05）. Conclusions： SalB increases the level of antioxidant substances and decreases free radicals production. Moreover, it also improves Bcl-2 expression and reduces Bax expression. SalB may exert the neuroprotective effect through mitochondria-dependent pathway on hippocampal CA1 neurons in mice with cerebral ischemia and reperfusion injury and suggested that SalB represents a promising candidate for the prevention and treatment of ischemic cerebrovascular disease.

关 键 词：Salvianolic acid B ISCHEMIA-REPERFUSION HIPPOCAMPUS NEURON apoptosis 

分 类 号：R285.5[医药卫生—中药学]