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.
"Recent studies have suggested that β-asarone is one of the main bioactive constituents of its essential oil. Growing evidence has demonstrated that β-asarone has the properties of antifungal (Lee et al., 2004) and anthelmintic activity (Lee et al., 2008; Kumar et al., 2009), modulating neurotransmission (Qiu et al., 2011), blocking cholesterol biosynthesis (Lee et al., 2010) and tranquilization or central inhibitory activity (Liao et al., 1998; Fang et al., 2008). However, little is known about its inhibitory effect on cancer cells and the precise mechanism behind it remains unclear. "
[Show abstract][Hide abstract] ABSTRACT: Beta-asarone is one of the main bioactive constituents in traditional Chinese medicine Acorus calamu. Previous studies have shown that it has antifungal and anthelmintic activities. However, little is known about its anticancer effects. This study aimed to determine inhibitory effects on LoVo colon cancer cell proliferation and to clarify the underlying mechanisms in vitro and in vivo. Dose-response and time-course anti-proliferation effects were examined by MTT assay. Our results demonstrated that LoVo cell viability showed dose- and time-dependence on β-asarone. We further assessed anti-proliferation effects as β-asarone-induced apoptosis by annexin V-fluorescein isothiocyanate/propidium iodide assay usinga flow cytometer and observed characteristic nuclear fragmentation and chromatin condensation of apoptosis by microscopy. Moreover, we found the apoptosis to be induced through the mitochondrial/caspase pathway by decreasing mitochondrial membrane potential (MMP) and reducing the Bcl-2-to-Bax ratio, in addition to activating the caspase-9 and caspase-3 cascades. Additionally, the apoptosis could be inhibited by a pan-caspase inhibitor, carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone (Z-VAD-FMK). When nude mice bearing LoVo tumor xenografts were treated with β-asarone, tumor volumes were reduced and terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) assays of excised tissue also demonstrated apoptotic changes. Taken together, these findings for the first time provide evidence that β-asarone can suppress the growth of colon cancer and the induced apoptosis is possibly mediated through mitochondria/caspase pathways.
Asian Pacific journal of cancer prevention: APJCP 10/2012; 13(10):5291-8. DOI:10.7314/APJCP.2012.13.10.5291 · 2.51 Impact Factor
"Autophagy, a process of self-eating, is usually induced by starvation, ischemia and hypoxia, growth factor deficiency, etc. It helps to maintain cell homeostasis1, 2, 3, but excessive autophagy may also leads to autophagic neuron death and apoptosis4, 5, 6. β-asarone, one of chief constituents from Acorus Tatarinowii Schott, can easily pass through the blood brain barrier7, and shows various neuroprotective effects such as protecting neuron against apoptosis8, 9, 10, 11. However, the effect of β-asarone on autophagy in a model of ischemic stroke in vitro is rarely reported. "
[Show abstract][Hide abstract] 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.
"It has been reported that ␤-asarone could attenuate neuronal apoptosis in rat hippocampus and might be a potential candidate for development as a therapeutic agent to manage cognitive impairment associated with conditions such as Alzheimer's disease (Li et al. 2010; Liu et al. 2010). Other authors found ␤-asarone could reduce the toxicity of excitatory amino acids in the epileptic rat brain and increase the expression of c-fos (Fang et al. 2008). Additionally, ␤-asarone could reduce the injuries of blood vessel endothelium and nerve cells of the cortex (Fu et al. 2008; Chen et al. 2007) and improve the cognitive function of the beta-amyloid hippocampus injection rats (Geng et al. 2010). "
[Show abstract][Hide abstract] ABSTRACT: beta-Asarone has significant pharmacological effects on the central nervous system. As a potential therapeutic agent to manage brain diseases, analysis of the pharmacokinetics of beta-asarone in brain is necessary. We used cardio-perfusion method to exclude the beta-asarone in the brain blood. The brain was divided into five regions: hippocampus, cortex, brain stem, thalamus and cerebellum, and pharmacokinetic differences were investigated. We found that concentration-time profile of beta-asarone in blood, hippocampus, cortex, brain stem and cerebellum could be adequately described by a first-order equation, consistent with a linear two-compartmental model, but a first-order equation with a linear one-compartmental model in thalamus. The half lives of beta-asarone in blood, hippocampus, cortex, brain stem, thalamus and cerebellum were 1.3801, 1.300, 1.937, 7.142, 2.832 and 8.149 h, respectively. Gender differences do not significantly influence plasma pharmacokinetics of beta-asarone.
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