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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 4groups with 10 animals each,including the sham group,the model group,the SaIB group(SaIB 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 min followed by 24-h reperfusion.The malondialdehyde(MDA) content,the nitric oxide synthase(NOS) activity,the superoxide dismutase(SOD) activity and total antioxidant 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 hematoxylineosin staining and immunohistochemistry staining,respectively.Results:In the SaIB 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 SaIB 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:SaIB increases the level of antioxidant substances and decreases free radicals production.Moreover,it also improves Bcl-2 expression and reduces Bax expression.SaIB may exert the neuroprotective effect through mitochondria-dependent pathway on hippocampal CA1 neurons in mice with cerebral ischemia and reperfusion injury and suggested that SaIB 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 mice with the sham group, the model group, the SaIB group (SaIB 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 min followed by 24-h reperfusion. The malondialdehyde (MDA) content, the nitric oxide synthase (NOS) activity, the superoxide dismutase (SOD) activity and total antioxidant 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 hematoxylineosin staining and immunohistochemistry staining, respectively. Results: I n the SaIB 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) (P <0.01) and inhibited Bax protein expression (P <0.05) .Conclusions: SaIB increases the level of antioxidant (P <0.01) in the hippocampal CA1 region, strongly promoted Bcl- substances and decreases free radicals production. Moreover, it also improves Bcl-2 expression and reduces Bax expression. SAIB may exert the neuroprotective effect through mitochondria-dependent pathway on hippocampal CA1 neurons in mice with cerebral ischemia and reperfusion injury and suggested that SaIB represents a promising candidate for the prevention and treatment of ischemic cerebrovascular disease.