Effect of schizandra B on reorganization of primary hippocampus neurons dendritic spine induced by epilepsy

Abstract

Abstract:To investigate the effect of schizandra B(Sch B) on reorganization of primary hippocampus cells dendritic spines induced by Glu. Methods: The primary hippocampus cells were divided into control group, model group and Sch B group. The primary cells in control group were untreated; the primary cells in model group were treated with Glu(15mmol.L-1)for 24h. The primary cells in Sch B group were firstly pretreated with Sch B （0.5μmmol.L-1） for 2h, and exposed to Glu(15mmol.L-1)for 24h. Results: A significant decrease of spines in number was found in the model group cells（3± 2.0/ 10μm n=12） when compared whose those in the control（12± 3.0/μm n=10，p<0.01,t-test）. A slightly decrease of spines in number were found in cells of Sch B group (8± 2.0/ 10μm n=12). Western blot analysis revealed that there is no effect on the total levels of actin and cofilin; However, it can decrease the levels of p-cofilin in the model group. The levels of p-cofilin in Sch B Group is higher than those in model group. Conclusion: Sch B can protect the damage of dendritic spines caused by Glu that is related to inhibit the activation of p-cofilin.Patients with epilepsy often have cognitive impairment due to epilepsy itself [1][2][3][4]. Seizures can cause mild changes in dendritic morphology and dendritic spine of neurons. Dendritic spines is neuronal excitatory postsynaptic component. The number of dendritic spines of hippocampus and neocortex that is related to memory and cognition were decreased in the patient of epilepsy. We hypothesis abnormal dendritic spines maybe causes cognitive damage. [5][6].The changes of the cytokines skeleton changes in glutamate activation are related to the seizure. Glutamate antagonist can prevent the decrease number of dendritic spines caused by seizures. Glutamate agonists kainic acid induced seizures cause the decrease in the number of dendritic spines in hippocampal CA1 area and the neocortex, which is caused by depolymerization of actin cytoskeleton cofilin [14]. At present, epilepsy is mainly controlled by antagonism of neurotransmitters or by blocking ion channels. This study attempts to treat epilepsy by stabilizing the intra-synaptic actin skeleton Schisandra is a traditional Chinese medicine, which play roles in central inhibition and the role of tranquilization [15]. Studies have shown that schizandrine can prevent glutamate induced neuronal damage and antioxidation [10][11]. It not only effectively prevents the damage of the oxidative stress induced by glutamate in the rat brain, but also improves the memory function of mice by regulating the level of acetylcholine. It also promoted dendritic growth and synaptic formation in