[Effects of beta-asarone on expression of c-fos in kindling epilepsy rat brain].
ABSTRACT To study the effects of beta-asarone on expression of immediately early gene c-fos in kindling epilepsy rat brain.
The rats were randomly divided in to beta-asarone groups (200, 100, 50 mg x kg(-1) x d(-1)), difetoin control group (36 mg x kg(-1)) and model group. The remedy was administered orally. The effects were observed in kindling epilepsy model induced by penicillin, then the expression of c-fos were determined by western blot (hippocampus) and immunohistochemical techniques (cortex).
Beta-asarone could significantly increase the expression of c-fos in kindling epilepsy rat brain, and show its quantity-effect relation. The expression of c-fos in hippocampus was (1139.45 +/- 155.56), (1109.56 +/- 134.03), (1103.73 +/- 235.82) CNT x mm2 in beta-asarone groups, 920.54 +/- 203.20 in model control group, and 1106.26 +/- 186.24 in difetoin group, respectively. The number of c-fos positive cell was 87.1 +/- 2.2, 76.3 +/- 1.3 and 59.9 +/- 1.3 in beta-asarone groups, 39.3 +/- 2.6 in model control group, and 95.2 +/- 1.1 in difetoin group, respectively.
Beta-asarone can obviously increase the expression of c-fos in epilepsy rat brain. It is one of important response to epilepsy.
- SourceAvailable from: Byung-Wook Kim07/2014;
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ABSTRACT: Ischemic hypoxic brain injury often causes irreversible brain damage. The lack of effective and widely applicable pharmacological treatments for ischemic stroke patients may explain a growing interest in traditional medicines. beta-Asarone, which has significant pharmacological effects on the central nervous system (CNS), was used in the prevention of cerebral ischemia in this paper. The right middle cerebral artery occlusion model was used in the study. The effects of beta-Asarone on mortality rate, neurobehavior, grip strength, lactate dehydrogenase, glutathione content, Lipid peroxidation, glutathione peroxidase activity, glutathione reductase activity, catalase activity, Na+-K+-ATPase activity and glutathione S transferase activity in a rat model were studied respectively. beta-Asarone significantly improved the neurological outcome after cerebral ischemia and reperfusion in terms of neurobehavioral function in rats. Meanwhile, supplementation of beta-Asarone significantly boosted the defense mechanism against cerebral ischemia via increasing antioxidants activity related to lesion pathogenesis. Restoration of the antioxidant homeostasis in the brain after reperfusion may help the brain recover from ischemic injury. These experimental results suggest that complement beta-Asarone is protective against cerebral ischemia in specific way. The administration of beta-Asarone could reduce focal cerebral ischemic/reperfusion injury. The Mechanism of beta-Asarone in protection of cerebral ischemia was via increasing antioxidants activity related to lesion pathogenesis.BMC Complementary and Alternative Medicine 09/2013; 13(1):236. · 2.08 Impact Factor
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ABSTRACT: To explore the effects of β-asarone from Acorus Tatarinowii Schott on autophagy in an ischemic stroke model of PC12 cells. The ischemic stroke model of PC12 cells was made by OGD/R (2 h oxygen-glucose deprivation followed by 24 h reperfusion). Drug administration was started 1 h before OGD and last for 3 h. Then the cells were incubated in the drug-free and full culture medium under normoxic conditions for 24 h. After the treatments, Beclin-1, intracellular free calcium concentration ([Ca(2+)](i)) and mitochondrial membrane potential (MMP) were analyzed using flow cytometry. Cell viability was measured using MTT assay. Cell morphology was studied under inverted phase contrast microscope, and autophagosomes were observed under transmission electron microscope. Pretreatment with β-asarone (20, 30, or 45 μg/mL) or the calcium channel antagonist nimodipine (10 μmol/L) significantly increased the cell viability and MMP, and decreased Beclin-1 expression and [Ca(2+)](i) in OGD/R-treated PC12 cells. Under inverted phase contrast microscope, pretreatment with β-asarone or nimodipine dramatically increase the number of cells and improved the cellular morphology. Autophagosomes were found in OGD/R-treated PC12 cells as well as in drug plus OGD/R-treated PC12 cells. β-Asarone protects PC12 cells against OGD/R-induced injury partly due to attenuating Beclin-1-dependent autophagy caused by decreasing [Ca(2+)](i) and increasing MMP.Acta Pharmacologica Sinica 04/2012; 33(6):737-42. · 2.35 Impact Factor