[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 Kim[Show abstract] [Hide abstract]
ABSTRACT: Acorus species contains diverse pharmacologically active phytochemicals including α-asarone, β-asarone, and eugenol. We determined if β-asarone isolated from Acorus gramineus (AG) Solander would be efficacious in protecting BV-2 microglia cells from lipopolysaccharide (LPS)-induced stress signaling. BV-2 microglial cells were pretreated with an AG ethanol extract (1, 10, and 100 μg/mL) or β-asarone (10, 50, and 100 μM) prior to exposure to LPS (100 ng/mL). AG and β-asarone inhibited LPS-induced production of nitric oxide in a dose-dependent manner. The mRNA and protein levels of inducible nitric oxide synthase and cyclooxygenase-2 also decreased dose dependently following AG and β-asarone treatments. Immunostaining and immunoblot studies revealed that β-asarone also suppressed nuclear factor (NF)-κB activation by blocking IkB degradation. Further mechanistic studies revealed that β-asarone acted through the JNK/MAPK pathway. Taken together, our findings demonstrate that β-asarone exhibits anti-inflammatory effects by suppressing the production of pro-inflammatory mediators through NF-κB signaling and the JNK pathways in activated microglial cells and might be developed as a promising candidate to treat various neuroinflammatory diseases.Food and Chemical Toxicology 07/2014; 72. · 2.61 Impact Factor
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ABSTRACT: Alzheimer's disease (AD) is an age related and progressive neurodegenerative disease. Autophagy is a self-degradative process and plays a critical role in removing long-lived proteins and damaged organelles. Recent evidence suggests that autophagy might be involved in the pathogenesis of AD. β-asarone have various neuroprotective effects. However, the effect of β-asarone on autophagy in amyloid β-peptide (Aβ) induced cell injury is unclear, and little is known about the signaling pathway of β-asarone in autophagy regulation. The aim of the present study was to determine whether β-asarone protects cells from Aβ1-42 induced cytotoxicity via regulation of Beclin-1 dependent autophagy and its regulating signaling pathway. We examined effects of β-asarone on cell morphology, cell viability, neuron specific enolase (NSE) levels, autophagosomes and regulating Beclin-1, p-Akt, p-mTOR expression in Aβ1-42 treated PC12 cells. We found that β-asarone could maintain the original morphology of cells and increase cell viability and decrease NSE levels significantly. Meanwhile, β-asarone decreased Beclin-1 expression significantly. In addition, β-asarone can increase levels of p-Akt and p-mTOR. These results showed that β-asarone protected cells from Aβ1-42 induced cytotoxicity and attenuated autophagy via activation of Akt-mTOR signaling pathway, which could be involved in neuroprotection of β-asarone against Aβ toxicity. Our findings suggest that β-asarone might be a potential preventive drug for AD.European Journal of Pharmacology 08/2014; · 2.68 Impact Factor