|Source:||The herbs of Asarum sieboldii Miq.|
|Biological Activity or Inhibitors:||1. Beta-Asarone may be a potential preventive drug for Alzheimer's disease.
2. Beta-Asarone prevents autophagy and synaptic loss by reducing ROCK expression in SAMP8 mice.
3. The co-administration of beta-Asarone and l-dopa may contribute to the treatment of 6-OHDA-induced damage in rats by inhibiting autophagy activity.
4. Beta-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.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||4.8008 mL||24.0038 mL||48.0077 mL||96.0154 mL||120.0192 mL|
|5 mM||0.9602 mL||4.8008 mL||9.6015 mL||19.2031 mL||24.0038 mL|
|10 mM||0.4801 mL||2.4004 mL||4.8008 mL||9.6015 mL||12.0019 mL|
|50 mM||0.096 mL||0.4801 mL||0.9602 mL||1.9203 mL||2.4004 mL|
|100 mM||0.048 mL||0.24 mL||0.4801 mL||0.9602 mL||1.2002 mL|
Clin Exp Pharmacol Physiol. 2015 Mar;42(3):269-77.
|β-asarone and levodopa co-administration protects against 6-hydroxydopamine-induced damage in parkinsonian rat mesencephalon by regulating autophagy: down-expression Beclin-1 and light chain 3B and up-expression P62.[Pubmed: 25424835]|
|In this study, we investigated Beclin-1, light chain (LC)3B, and p62 expression in 6-hydroxydopamine (6-OHDA)-induced parkinsonian rats after beta-Asarone and levodopa (l-dopa) co-administration. Unilateral 6-OHDA injection into the medial forebrain bundle was used to create the models, except in sham-operated rats. Rats were divided into eight groups: sham-operated group; 6-OHDA model group; madopar group (75 mg/kg, per os (p.o.)); l-dopa group (60 mg/kg, p.o.); beta-Asarone group (15 mg/kg, p.o.); beta-Asarone + l-dopa co-administered group (15 mg/kg + 60 mg/kg, p.o.); 3-methyladenine group (500 nmol, intraperitoneal injection); and rapamycin group (1 mg/kg, intraperitoneal injection). Then, Beclin-1, LC3B, and p62 expression in the mesencephalon were detected. The mesencephalon was also observed by transmission electron microscope. The results showed that Beclin-1 and LC3B expression decreased and that p62 expression increased significantly in the madopar, l-dopa, beta-Asarone, and co-administered groups when compared with the 6-OHDA model. Beclin-1 and LC3B expression in the beta-Asarone and co-administered groups were less than in the madopar or l-dopa groups, whereas p62 expression in the beta-Asarone and co-administered groups was higher than in the madopar or l-dopa groups. In addition, a significant decrease in autophagosome was exhibited in the beta-Asarone and co-administered groups when compared with the 6-OHDA group. Our findings indicate that Beclin-1 and LC3B expression decreased, whereas p62 expression increased after co-administration treatment. In sum, all data suggest that the co-administration of beta-Asarone and l-dopa may contribute to the treatment of 6-OHDA-induced damage in rats by inhibiting autophagy activity.|
Food Chem Toxicol. 2014 Oct;72:265-72.
|β-Asarone (cis-2,4,5-trimethoxy-1-allyl phenyl), attenuates pro-inflammatory mediators by inhibiting NF-κB signaling and the JNK pathway in LPS activated BV-2 microglia cells.[Pubmed: 25066769]|
|Acorus species contains diverse pharmacologically active phytochemicals including α-asarone, beta-Asarone, and eugenol. We determined if beta-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 beta-Asarone (10, 50, and 100 μM) prior to exposure to LPS (100 ng/mL). AG and beta-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 beta-Asarone treatments. Immunostaining and immunoblot studies revealed that beta-Asarone also suppressed nuclear factor (NF)-κB activation by blocking IkB degradation. Further mechanistic studies revealed that beta-Asarone acted through the JNK/MAPK pathway. Taken together, our findings demonstrate that beta-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.|
Eur J Pharmacol. 2014 Oct 15;741:195-204.
|Beta-asarone attenuates amyloid beta-induced autophagy via Akt/mTOR pathway in PC12 cells.[Pubmed: 25160744]|
|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. beta-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 beta-Asarone protects cells from Aβ1-42 induced cytotoxicity via regulation of Beclin-1 dependent autophagy and its regulating signaling pathway. We examined effects of beta-Asarone on cell morphology, cell viability, neuron specific enolase (NSE) levels, autophagosomes and regulating Beclin-1, p-Akt and p-mTOR expressions in Aβ1-42 treated PC12 cells. We found that beta-Asarone could maintain the original morphology of cells and increase cell viability and decrease NSE levels significantly. Meanwhile, beta-Asarone decreased Beclin-1 expression significantly. In addition, beta-Asarone can increase levels of p-Akt and p-mTOR. These results showed that beta-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 beta-Asarone against Aβ toxicity. Our findings suggest that beta-Asarone might be a potential preventive drug for AD.|
Brain Res. 2014 Mar 13;1552:41-54.
|β-Asarone prevents autophagy and synaptic loss by reducing ROCK expression in asenescence-accelerated prone 8 mice.[Pubmed: 24457043]|
|beta-Asarone is an active component of the Acori graminei rhizome that is a traditional Chinese medicine clinically used in treating dementia in China. However, the cognitive effect of beta-Asarone and its mechanism has remained elusive. Here, we used asenescence-accelerated prone 8 (SAMP8) mice, which mimic many of the salient features of Alzheimer׳s disease (AD), to further investigate whether modulation of the ROCK signaling pathway and/or autophagy, synaptic loss is involved in the effects of beta-Asarone on learning and memory. SAMP8 mice at the age of 6 months were intragastrically administered by beta-Asarone or a vehicle daily for 2 months. Senescence-accelerated-resistant (SAMR1) mice were used as the control. Our results demonstrate that autophagy and ROCK expression were increased significantly in 8 months SAMP8 mice, which were concomitant with that SAMP8 mice at the same age displayed a significant synaptic loss and cognitive deficits. The up-regulation of ROCK expression and autophage in the hippocampus of SAMP8 were significantly reduced by beta-Asarone, and prevents synaptic loss and improved cognitive function of the SAMP8 mice. beta-Asarone decreased neuronophagia and lipofuscin in the hippocampus of SAMP8 mice, but did not reduce Aβ42 levels and malondialdehyde levels and superoxide dismutase activities. Moreover, suppression of ROCK2 by siRNA significantly reduced the effects of beta-Asarone on the autophage and synaptic proteins expression in PC12 cells damage induced by Aβ1-40. Taken together, beta-Asarone prevents autophagy and synaptic loss by reducing ROCK expression in SAMP8 mice.|