The effects of salvianolic acid B (SalB) on the mitochondrial membrane potential (MMP), calcium, and apoptosis of neurons with cerebral ischemia in mice were investigated using an acute cerebral ischemia model established by ligating the bilateral common carotid arteries in mice. The MMP, the intracellular calcium concentration, and the apoptosis rate of cortical neurons were measured at 6 min, 12 min, 18 min, 24 min, and 30 min after cerebral ischemia by a flow cytometer. The experiments show that SalB increases the MMP and reduces the intracellular calcium and the apoptosis rate at different stages of the cerebral ischemia in mice. The results show that the protective mechanism of SalB on cerebral ischemia enhances the MMP and maintains intracellular calcium homeostasis.
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.
