beta-Asarone

Compositional variations and anthelmentic activity of essential oils from rhizomes of different wild populations of Acorus calamus L. and its major component, beta-Asarone.[Pubmed: 19370938]

Nat Prod Commun. 2009 Feb;4(2):275-8.

Hydro-distilled essential oils from Acorus calamus rhizomes collected from six different geographical zones in the northwest Himalayan region of Uttarakhand have been analyzed by GC and GC/MS.
METHODS AND RESULTS:
All the oils differed in their qualitative and quantitative make up, although beta-Asarone was the major constituent of all of them. The essential oils and the isolated beta-Asarone were screened for anthelmintic activity using contractility of Ascaridia galli. beta-Asarone, in particular, showed potent activity with IC50 values of 75.4 +/- 61.8 ng/mL.

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]

Food Chem Toxicol. 2014 Oct;72:265-72.

Acorus species contains diverse pharmacologically active phytochemicals including α-asarone, beta-Asarone, and eugenol.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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.

β-Asarone induces senescence in colorectal cancer cells by inducing lamin B1 expression.[Pubmed: 23357361 ]

Phytomedicine. 2013 Apr 15;20(6):512-20.

Colorectal cancer is a leading cause of cancer mortality with a complex carcinogenesis that includes reduced cellular senescence. Lamin proteins are decreased in senescing cells, and frequently decreased in malignancies.
METHODS AND RESULTS:
This study identified a new drug candidate for colorectal cancer that appears to target cell senescence via a lamin protein. beta-Asarone (1-propenyl-2,4,5-methoxybenzol) is a compound from the traditional medical herb Acorus calamus Linn. This study tested the in vitro and in vivo effects of beta-Asarone on colorectal cancer cells by testing cell viability using human colorectal cell lines HT29 and SW480 in MTT assays; tumorigenesis using xenografts in nude mice and a mouse model of colorectal cancer; cell senescence using senescence-associated β-galactosidase activity; and expression of cancer and senescence-related proteins, specifically lamins, Oct-1, p53, p21, and p15, by Western blot. beta-Asarone appeared to increase expression of lamin B1, p53, p21, but not lamin A/C. beta-Asarone regulates p15 expression by regulation of Oct-1 binding.
CONCLUSIONS:
Collectively, the results suggested that beta-Asarone inhibits colon cancer formation in vivo and in vitro by inducing senescence. Since beta-Asarone induced lamin B1 expression, a model is proposed in which beta-Asarone inhibits colorectal cancer by inducing senescence through lamin B1.

Beta-asarone attenuates amyloid beta-induced autophagy via Akt/mTOR pathway in PC12 cells.[Pubmed: 25160744]

Eur J Pharmacol. 2014 Oct 15;741:195-204.

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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
Our findings suggest that beta-Asarone might be a potential preventive drug for AD.

Assessing reproductive toxicity and antioxidant enzymes on beta asarone induced male Wistar albino rats: In vivo and computational analysis.[Pubmed: 27569590 ]

The anticoagulant effect of beta-asarone in the mouse and the rat.[Pubmed: 1788271]

Proc West Pharmacol Soc. 1991;34:107-12.

The anticoagulant effect of beta-Asarone in the mouse and the rat.

Life Sci. 2017 Mar 15;173:150-160.

beta-Asarone is the major constituent of oil obtained from Acorus calamus, the Indian traditional medicine plant. Several studies have shown that beta-Asarone causes liver and cardiac damages but the reproductive toxicity is not well understood. The present study was initiated to investigate whether beta-Asarone has the potential to cause reproductive toxicity by inducing oxidative stress in the testis of male Wistar albino rats.
METHODS AND RESULTS:
For this study, the animals were divided into six groups: Group I was treated with saline (normal saline), Group II with DMSO (vehicle control) and Group III with cisplatin (10mg/kgb.wt.). Group IV, V and VI animals were administrated at three dose levels of beta-Asarone 12.5, 25 and 50mg/kgb.wt. The treatment was carried out for 14days and animals were sacrificed on 29th day and processed for sperm analysis, hormone assay, histopathological, and antioxidant enzymatic assays. We also used molecular docking studies to predict the binding nature of beta-Asarone with luteinizing hormone receptor (LHR) and follicle-stimulating hormone receptor (FSHR). beta-Asarone administered at a dose of 50mg/kgb.wt. was responsible for inducing certain noticeable degenerative changes in histopathological analysis of the tissue. This was supported by altered sperm morphology and hormonal variations when compared to the control groups. Antioxidant enzyme levels were also found to be decreased. This was further validated by molecular docking studies.
CONCLUSIONS:
The present study provides evidence that beta-Asarone administered at a dose of 50mg/kg b.wt. is capable enough in bringing about moderate amount of degenerative changes in rat testis and altered antioxidant status. Therefore provides a suitable evidence to prove that beta-Asarone causes reproductive toxicity.