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Yong-qi Fang - One of the best experts on this subject based on the ideXlab platform.

  • Beta-Asarone Reduces Autophagy in a Dose-Dependent Manner and Interferes with Beclin 1 Function
    Autophagy: Cancer Other Pathologies Inflammation Immunity Infection and Aging, 2015
    Co-Authors: Yong-qi Fang, Zhong-feng Xue
    Abstract:

    Beta-Asarone, extracted from Acorus tatarinowii Schott, has significant pharmacological effects on the central nervous system (CNS). Beta-Asarone can pass through the blood–brain barrier and then enter into the brain. The absorption, distribution, and elimination of Beta-Asarone are rapid and it is found in low accumulations in the body. Brain is an important organ of distribution. Beta-Asarone is quickly excreted in urine, feces, and bile, but the excretion efficiency in urine is the highest. Beta-Asarone could attenuate neuronal autophagy. We examined effects of gradient concentrations of Beta-Asarone on autophagy and found that a high dose has a stronger effect than that of a low dose. Beta-Asarone reduces autophagy in a dose-dependent manner. In view of the close relationship between Beclin 1 and autophagy, we found that Beta-Asarone interfered with Beclin 1 function. Our studies on the mechanism by which Beta-Asarone attenuates autophagy indicate that it is likely that Beta-Asarone can modulate JNK, p-JNK, Bcl-2, and Beclin 1. Also, autophagy induced by increased intracellular free calcium concentration ([Ca2+]i) and decreased mitochondrial membrane potential (MMP) in oxygen-glucose deprivation and reperfusion (OGD/R)-treated PC12 cells was detected. Beta-Asarone significantly increased cell viability and MMP, and improved cellular morphology but decreased Beclin 1 and [Ca2+]i. Along with the development of research, more and more mechanisms of Beta-Asarone are being found in relation to the regulation of autophagy. This helps us to understand more deeply the significance of Beta-Asarone in treatment of disease.

  • Beta Asarone attenuates amyloid Beta induced autophagy via akt mtor pathway in pc12 cells
    European Journal of Pharmacology, 2014
    Co-Authors: Zhong-feng Xue, Ruo-ming Fang, Yalei Guo, Sheng Zhang, Liping Huang, Yong-qi Fang
    Abstract:

    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 and p-mTOR expressions 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.

  • Beta-Asarone attenuates amyloid Beta-induced autophagy via Akt/mTOR pathway in PC12 cells.
    European journal of pharmacology, 2014
    Co-Authors: Zhong-feng Xue, Ruo-ming Fang, Yalei Guo, Sheng Zhang, Liping Huang, Yong-qi Fang
    Abstract:

    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 and p-mTOR expressions 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.

  • Beta-Asarone attenuates ischemia-reperfusion-induced autophagy in rat brains via modulating JNK, p-JNK, Bcl-2 and Beclin 1.
    European journal of pharmacology, 2012
    Co-Authors: Lin Liu, Yong-qi Fang, Zhong-feng Xue, Ruo-ming Fang
    Abstract:

    Beta-Asarone has significant pharmacological effects on the central nervous system. It can attenuate neuronal apoptosis, but its effects on the brain ischemia-reperfusion-induced autophagy have not been reported yet. Our study was a two-stage procedure: evaluation of β-Asarone effects on the autophagy at first, and then analysis of the possible mechanism. The middle cerebral artery occlusion (MCAO) model was adopted to make the brain injure and Beclin 1 was used to evaluate the autophagy. We hypothesized that the mechanism might be related to c-Jun N-terminal kinases (JNK), phospho-JNK (p-JNK), Bcl-2 and Beclin 1. To test this hypothesis, we evaluated JNK, p-JNK, Bcl-2 and Beclin 1 levels with flow cytometry. Additionally, we divided the brain into three regions: ischemic region, ischemic penumbra, and normal region, and analyzed them respectively. We found, compared to both groups II (model control) and III (low dose), Beclin 1 levels in groups IV (medium dose) and V (high dose) were significantly decreased. Beclin 1, JNK and p-JNK levels in groups VII (β-Asarone) and VIII (JNK inhibitor) were significantly decreased, but Bcl-2 levels were significantly increased. Additionally, Beclin 1, JNK, p-JNK and Bcl-2 levels among the three regions had no significant differences. We conclude that β-Asarone can attenuate the autophagy in a dose-dependent manner. The mechanism is likely that β-Asarone can decrease JNK and p-JNK levels at first, and then increase Bcl-2 level, finally interfere with the functions of Beclin 1 during the execution of autophagy. Additionally, β-Asarone can attenuate autophagy in a widespread manner.

  • Beta-Asarone attenuates ischemia–reperfusion-induced autophagy in rat brains via modulating JNK, p-JNK, Bcl-2 and Beclin 1
    European Journal of Pharmacology, 2012
    Co-Authors: Lin Liu, Yong-qi Fang, Zhong-feng Xue, Ruo-ming Fang
    Abstract:

    Beta-Asarone has significant pharmacological effects on the central nervous system. It can attenuate neuronal apoptosis, but its effects on the brain ischemia-reperfusion-induced autophagy have not been reported yet. Our study was a two-stage procedure: evaluation of β-Asarone effects on the autophagy at first, and then analysis of the possible mechanism. The middle cerebral artery occlusion (MCAO) model was adopted to make the brain injure and Beclin 1 was used to evaluate the autophagy. We hypothesized that the mechanism might be related to c-Jun N-terminal kinases (JNK), phospho-JNK (p-JNK), Bcl-2 and Beclin 1. To test this hypothesis, we evaluated JNK, p-JNK, Bcl-2 and Beclin 1 levels with flow cytometry. Additionally, we divided the brain into three regions: ischemic region, ischemic penumbra, and normal region, and analyzed them respectively. We found, compared to both groups II (model control) and III (low dose), Beclin 1 levels in groups IV (medium dose) and V (high dose) were significantly decreased. Beclin 1, JNK and p-JNK levels in groups VII (β-Asarone) and VIII (JNK inhibitor) were significantly decreased, but Bcl-2 levels were significantly increased. Additionally, Beclin 1, JNK, p-JNK and Bcl-2 levels among the three regions had no significant differences. We conclude that β-Asarone can attenuate the autophagy in a dose-dependent manner. The mechanism is likely that β-Asarone can decrease JNK and p-JNK levels at first, and then increase Bcl-2 level, finally interfere with the functions of Beclin 1 during the execution of autophagy. Additionally, β-Asarone can attenuate autophagy in a widespread manner.

Minmin Shen - One of the best experts on this subject based on the ideXlab platform.

  • Systematic study of Beta-Asarone-rich volatile oil from Acori graminei rhizoma by off-line supercritical CO2 extraction-gas chromatography-mass spectrometry.
    Journal of separation science, 2008
    Co-Authors: Jian Dai, Minmin Shen
    Abstract:

    Supercritical CO2 extraction (SCE) technology was used to extract a volatile oil, rich in Beta-Asarone, from Acori graminei rhizoma (AGR). The effect of different extraction and fractionation parameters on oil yield and selectivity towards Beta-Asarone was investigated by SCE using commercial AGR samples. The optimal conditions (P(e)/T(e) = 10 MPa/45 degrees C; P(f1)/T(f1) = 8 MPa/-10 degrees C; P(f2)/T(f2 )= 2 MPa/10 degrees C) gave a good oil yield and selectivity for Beta-Asarone. The extracts were also analyzed by GC-MS and compared with the volatile oil obtained by hydrodistillation, in which 39 main constituents including Beta-Asarone were found. Different cultivated AGR samples obtained from three areas of China were evaluated in terms of their volatile oil compositions obtained by extraction of commercial AGR samples under optimal conditions; the extract of the Guangdong (GD) sample showed a high Beta-Asarone content.

Arun K. Sinha - One of the best experts on this subject based on the ideXlab platform.

  • Larvicidal and Structure-Activity Studies of Natural Phenylpropanoids and Their Semisynthetic Derivatives against the Tobacco Armyworm Spodoptera litura (FAB.) (Lepidoptera: Noctuidae)
    Chemistry & biodiversity, 2010
    Co-Authors: Anu Bhardwaj, Arun K. Sinha, Dhananjay Kumar Tewary, Rakesh Kumar, Vinod Kumar, Adarsh Shanker
    Abstract:

    The larvicidal activity of 18 phenylpropanoids, 1-18, including phenylpropenoate, phenylpropenal, phenylpropene, and their semisynthetic analogues, were evaluated against the tobacco armyworm, Spodoptera litura (FAB.), to identify promising structures with insecticidal activity. Amongst various phenylpropanoids, isosafrole, a phenylpropene, showed the best activity, with an LC(50) value of 0.6 mu g/leaf cm(2), followed by its hydrogenated derivative dihydrosafrole (LC(50)=2.7 mu g/leaf cm(2)). The overall larvicidal activity of various phenylpropene derivatives was observed in the following order: isosafrole (6) > dihydrosafrole (16) > safrole (12) > anethole (4) > methyl eugenol (11) > eugenol (13) >Beta-Asarone (8)> dihydroAsarone (18) > dihydroanethole (15). Dihydrosafrole might be a promising compound, although presenting a lower larvicidal activity than isosafrole, because of its better stability and resistance to oxidative degradation (due to the removal of the extremely reactive olefinic bond) in comparison to isosafrole. Such structure-activity relationship studies promote the identification of lead structures from natural sources for the development of larvicidal products against S. litura and related insect pests.

  • Indian Acorus calamus Linn.-not a tetraploid.
    2009
    Co-Authors: R K Ogra, Prashant Mohanpuria, Utkarsh Sharma, Mohit Sharma, Arun K. Sinha, Paramvir Singh Ahuja
    Abstract:

    Acorus calamus Linn. (family Araceae), commonly known as sweet flag or 'Bach' in India, is an important medicinal and aromatic plant. In the present study, different accessions across the country were screened for ploidy status and possible correlation with Beta-Asarone content. Most of the accessions were triploids with Beta-Asarone content varying from 82.0 to 89.4% in their oil, except for only one triploid accession having 11.55% Beta-Asarone content. Two diploid populations were also detected from western Himalayas which had low Beta-Asarone contents of 11.67 and 7.39% respectively. The earlier notion that high Beta-Asarone content in the Indian calamus was due to its tetraploid status does not hold true cytologically. Amongst phenotypic characters, lower specific leaf weight values, early autumn senescence and late emergence in spring in a population can be indicators for locating accessions with low Beta-Asarone contents.

  • Ultrasound-assisted conversion of toxic Beta-Asarone into nontoxic bioactive phenylpropanoid: isoacoramone, a metabolite of Piper marginatum and Acorus tararinowii.
    Natural product research, 2004
    Co-Authors: Arun K. Sinha, Bhupendra P. Joshi, Arundhati Sharma, Harish Chandra Goel, Jagdish Prasad
    Abstract:

    Ultrasound-assisted synthesis of bioactive isoacoramone (1), a metabolite of Piper marginatum and Acorus tararinowii, has been achieved by oxidation of toxic β-Asarone (2) with potassium permanganate/copper sulphate/alumina into asaronaldehyde (3) followed by treatment with ethylmagnesium iodide to provide 1-(2,4,5-trimethoxy)phenyl-1-propanol (4) which upon further oxidation with potassium permanganate/copper sulphate afforded 1 in 64% yield (overall 32%). Toxicological evaluation of 1 reveals it to be nontoxic up to 60 mg/kg b.w.

Jagdish Prasad - One of the best experts on this subject based on the ideXlab platform.

Mohan S Karuppayil - One of the best experts on this subject based on the ideXlab platform.

  • an overview on traditional uses and pharmacological profile of acorus calamus linn sweet flag and other acorus species
    Phytomedicine, 2014
    Co-Authors: Sandeep B Rajput, Madan B Tonge, Mohan S Karuppayil
    Abstract:

    Acorus calamus (Sweet flag) has a long history of use and has numerous traditional and ethnomedicinal applications. Since ancient times, it has been used in various systems of medicines such as Ayurveda, Unani, Siddha, Chinese medicine, etc. for the treatment of various aliments like nervous disorders, appetite loss, bronchitis, chest pain, colic, cramps, diarrhea, digestive disorders, flatulence, gas, indigestion, rheumatism, sedative, cough, fever, bronchitis, inflammation, depression, tumors, hemorrhoids, skin diseases, numbness, general debility and vascular disorders. Various therapeutic potentials of this plant have been attributed to its rhizome. A number of active constituents from leaves, rhizomes and essential oils of A. calamus have been isolated and characterized. Of the constituents, alpha and Beta-Asarone are the predominant bioactive components. Various pharmacological activities of A. calamus rhizome such as sedative, CNS depressant, anticonvulsant, antispasmodic, cardiovascular, hypolipidemic, immunosuppressive, anti-inflammatory, cryoprotective, antioxidant, antidiarrheal, antimicrobial, anticancer and antidiabetic has been reported. Genotoxicity and mutagenecity of Beta and alpha-Asarone is reported, which limits their use at high dosage. Though A. calamus has been used since ancient times, many of its uses are yet to be scientifically validated. In the present review an attempt has been made to explore traditional uses and pharmacological properties of A. calamus.