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Chengguo Xing - One of the best experts on this subject based on the ideXlab platform.

  • A stable isotope dilution tandem mass spectrometry method of major kavalactones and its applications
    PLOS ONE, 2018
    Co-Authors: Yi Wang, Shainnel O. Eans, Heather M. Stacy, Sreekanth Narayanapillai, Linda G. Haddad, Jay P. Mclaughlin, Naomi Fujioka, Abhisheak Sharma, Bonnie A. Avery, Chengguo Xing
    Abstract:

    Kava is regaining its popularity with detailed characterizations warranted. We developed an ultraperformance liquid chromatography high-resolution tandem mass spectrometry (UPLC-MS/MS) method for major kavalactones (kavain, Dihydrokavain, methysticin, dihydromethysticin and desmethoxyyangonin) with excellent selectivity and specificity. The method has been validated for different matrices following the Food and Drug Administration guidance of analytical procedures and methods validation. The scope of this method has been demonstrated by quantifying these kavalactones in two kava products, characterizing their tissue distribution and pharmacokinetics in mice, and detecting their presence in human urines and plasmas upon kava intake. As expected, the abundances of these kavalactones differed significantly in kava products. All of them exhibited a large volume of distribution with extensive tissue affinity and adequate mean residence time (MRT) in mice. This method also successfully quantified these kavalactones in human body fluids upon kava consumption at the recommended human dose. This UPLC-MS/MS method therefore can be used to characterize kava products and its pharmacokinetics in animals and in humans.

  • Pilot in Vivo Structure–Activity Relationship of Dihydromethysticin in Blocking 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone-Induced O6-Methylguanine and Lung Tumor in A/J Mice
    Journal of Medicinal Chemistry, 2017
    Co-Authors: Manohar Puppala, Sreekanth C Narayanapillai, Pablo Leitzman, M. Gerard O'sullivan, Stephen S. Hecht, Pramod Upadhyaya, Chengguo Xing
    Abstract:

    (+)-Dihydromethysticin was recently identified as a promising lung cancer chemopreventive agent, while (+)-Dihydrokavain was completely ineffective. A pilot in vivo structure–activity relationship (SAR) was explored, evaluating the efficacy of its analogs in blocking 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced short-term O6-methylguanine and long-term adenoma formation in the lung tissues in A/J mice. Both results revealed cohesive SARs, demonstrating that the methylenedioxy functional group in DHM is essential while the lactone functional group tolerates modifications.

  • Pilot in Vivo Structure–Activity Relationship of Dihydromethysticin in Blocking 4‑(Methylnitrosamino)-1-(3-pyridyl)-1-butanone-Induced O6‑Methylguanine and Lung Tumor in A/J Mice
    2017
    Co-Authors: Manohar Puppala, Sreekanth C Narayanapillai, Pablo Leitzman, Stephen S. Hecht, Pramod Upadhyaya, Haifeng Sun, Gerard M. O’sullivan, Chengguo Xing
    Abstract:

    (+)-Dihydromethysticin was recently identified as a promising lung cancer chemopreventive agent, while (+)-Dihydrokavain was completely ineffective. A pilot in vivo structure–activity relationship (SAR) was explored, evaluating the efficacy of its analogs in blocking 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced short-term O6-methylguanine and long-term adenoma formation in the lung tissues in A/J mice. Both results revealed cohesive SARs, demonstrating that the methylenedioxy functional group in DHM is essential while the lactone functional group tolerates modifications

  • dihydromethysticin dhm blocks tobacco carcinogen 4 methylnitrosamino 1 3 pyridyl 1 butanone nnk induced o6 methylguanine in a manner independent of the aryl hydrocarbon receptor ahr pathway in c57bl 6 female mice
    Chemical Research in Toxicology, 2016
    Co-Authors: Sreekanth C Narayanapillai, Pablo Leitzman, Chengguo Xing, Carolyn J Baglole, Pramod Upadhyaya
    Abstract:

    4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a key carcinogen responsible for tobacco smoke-induced lung carcinogenesis. Among the types of DNA damage caused by NNK and its metabolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), O6-methylguanine (O6-mG) is likely the most carcinogen in A/J mice. Results of our previous studies showed that levels of O6-mG and other types of NNAL-derived DNA damage were preferentially reduced in the lung of female A/J mice upon dietary treatment with dihydromethysticin (DHM), a promising lung cancer chemopreventive agent from kava. Such a differential blockage may be mediated via an increased level of NNAL glucuronidation, thereby leading to its detoxification. The potential of the aryl hydrocarbon receptor (AhR) as an upstream target of DHM mediating these events was evaluated herein using Ahr+/– and Ahr–/– C57BL/6 female mice because DHM was reported as an AhR agonist. DHM (0.05, 0.2, and 1.0 mg/g of diet) and Dihydrokavain (DHK, an inactive analogue,...

Sreekanth C Narayanapillai - One of the best experts on this subject based on the ideXlab platform.

  • Pilot in Vivo Structure–Activity Relationship of Dihydromethysticin in Blocking 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone-Induced O6-Methylguanine and Lung Tumor in A/J Mice
    Journal of Medicinal Chemistry, 2017
    Co-Authors: Manohar Puppala, Sreekanth C Narayanapillai, Pablo Leitzman, M. Gerard O'sullivan, Stephen S. Hecht, Pramod Upadhyaya, Chengguo Xing
    Abstract:

    (+)-Dihydromethysticin was recently identified as a promising lung cancer chemopreventive agent, while (+)-Dihydrokavain was completely ineffective. A pilot in vivo structure–activity relationship (SAR) was explored, evaluating the efficacy of its analogs in blocking 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced short-term O6-methylguanine and long-term adenoma formation in the lung tissues in A/J mice. Both results revealed cohesive SARs, demonstrating that the methylenedioxy functional group in DHM is essential while the lactone functional group tolerates modifications.

  • Pilot in Vivo Structure–Activity Relationship of Dihydromethysticin in Blocking 4‑(Methylnitrosamino)-1-(3-pyridyl)-1-butanone-Induced O6‑Methylguanine and Lung Tumor in A/J Mice
    2017
    Co-Authors: Manohar Puppala, Sreekanth C Narayanapillai, Pablo Leitzman, Stephen S. Hecht, Pramod Upadhyaya, Haifeng Sun, Gerard M. O’sullivan, Chengguo Xing
    Abstract:

    (+)-Dihydromethysticin was recently identified as a promising lung cancer chemopreventive agent, while (+)-Dihydrokavain was completely ineffective. A pilot in vivo structure–activity relationship (SAR) was explored, evaluating the efficacy of its analogs in blocking 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced short-term O6-methylguanine and long-term adenoma formation in the lung tissues in A/J mice. Both results revealed cohesive SARs, demonstrating that the methylenedioxy functional group in DHM is essential while the lactone functional group tolerates modifications

  • dihydromethysticin dhm blocks tobacco carcinogen 4 methylnitrosamino 1 3 pyridyl 1 butanone nnk induced o6 methylguanine in a manner independent of the aryl hydrocarbon receptor ahr pathway in c57bl 6 female mice
    Chemical Research in Toxicology, 2016
    Co-Authors: Sreekanth C Narayanapillai, Pablo Leitzman, Chengguo Xing, Carolyn J Baglole, Pramod Upadhyaya
    Abstract:

    4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a key carcinogen responsible for tobacco smoke-induced lung carcinogenesis. Among the types of DNA damage caused by NNK and its metabolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), O6-methylguanine (O6-mG) is likely the most carcinogen in A/J mice. Results of our previous studies showed that levels of O6-mG and other types of NNAL-derived DNA damage were preferentially reduced in the lung of female A/J mice upon dietary treatment with dihydromethysticin (DHM), a promising lung cancer chemopreventive agent from kava. Such a differential blockage may be mediated via an increased level of NNAL glucuronidation, thereby leading to its detoxification. The potential of the aryl hydrocarbon receptor (AhR) as an upstream target of DHM mediating these events was evaluated herein using Ahr+/– and Ahr–/– C57BL/6 female mice because DHM was reported as an AhR agonist. DHM (0.05, 0.2, and 1.0 mg/g of diet) and Dihydrokavain (DHK, an inactive analogue,...

  • dihydromethysticin from kava blocks tobacco carcinogen 4 methylnitrosamino 1 3 pyridyl 1 butanone induced lung tumorigenesis and differentially reduces dna damage in a j mice
    Carcinogenesis, 2014
    Co-Authors: Sreekanth C Narayanapillai, Pablo Leitzman, Ahmad Ali Shaik, Gerard M Osullivan, Alex E. Grill, Silvia Balbo, Lisa A Peterson, Pramod Upadhyaya, Bo Zhou, Junxuan Lu
    Abstract:

    We have previously shown that kava and its flavokavain-free Fraction B completely blocked 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice with a preferential reduction in NNK-induced O 6-methylguanine (O 6-mG). In this study, we first identified natural (+)-dihydromethysticin (DHM) as a lead compound through evaluating the in vivo efficacy of five major compounds in Fraction B on reducing O 6-mG in lung tissues. (+)-DHM demonstrated outstanding chemopreventive activity against NNK-induced lung tumorigenesis in A/J mice with 97% reduction of adenoma multiplicity at a dose of 0.05mg/g of diet (50 ppm). Synthetic (±)-DHM was equally effective as the natural (+)-DHM in these bioassays while a structurally similar analog, (+)-Dihydrokavain (DHK), was completely inactive, revealing a sharp in vivo structure–activity relationship. Analyses of an expanded panel of NNK-induced DNA adducts revealed that DHM reduced a subset of DNA adducts in lung tissues derived from 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL, the active metabolite of NNK). Preliminary 17-week safety studies of DHM in A/J mice at a dose of 0.5mg/g of diet (at least 10× its minimum effective dose) revealed no adverse effects, suggesting that DHM is likely free of kava’s hepatotoxic risk. These results demonstrate the outstanding efficacy and promising safety margin of DHM in preventing NNK-induced lung tumorigenesis in A/J mice, with a unique mechanism of action and high target specificity.

Kenneth J. Sufka - One of the best experts on this subject based on the ideXlab platform.

  • Anxiolytic properties of Piper methysticum extract samples and fractions in the chick social-separation-stress procedure.
    Phytotherapy research : PTR, 2003
    Co-Authors: Matt W. Feltenstein, N.p. Dhammika Nanayakkara, Markus Ganzera, Ikhlas A. Khan, L. Corinne Lambdin, H. Ranjith, W. Dharmaratne, Kenneth J. Sufka
    Abstract:

    Piper methysticum extract (Kava kava) possesses anxiolytic properties. However, it is unknown whether these effects are best predicted by total kavalactone content or by one or more of its primary kavalactone constituents. Using the chick social separation-stress procedure as an anxiolytic bioassay, P. methysticum samples containing 12.8-100.0% total kavalactones (Exp. 1) and fractions containing 1-6 kavalactones of varying concentrations (0.1-67.5%; Exps. 2-3) were screened for activity and compared against a 5.0 mg/kg dose of chlordiazepoxide (CDP; Exp. 3). Eight-day-old chicks received IP injections of either vehicle or test compounds 30 min before being placed in the presence of two conspecifics or in isolation for a 3 min observation period. Dependent measures were ventral recumbency latency (sedation), distress vocalizations, and a measure of stress-induced analgesia (in Exps. 1 and 2 only). P. methysticum extract samples attenuated distress vocalizations in a concentration-dependent manner. The P. methysticum fraction that contained the highest concentration of Dihydrokavain attenuated distress vocalizations in a manner equivalent to that of CDP. The extract samples and fractions that possessed anxiolytic properties did not possess the sedative properties found in CDP. Collectively, these findings suggest that Dihydrokavain may be necessary and sufficient in mediating the anxiolytic properties of P. methysticum extract.

  • Anxiolytic effects of kava extract and kavalactones in the chick social separation-stress paradigm
    Psychopharmacology, 2001
    Co-Authors: Kenyatta K. Smith, Matt W. Feltenstein, Susan L. Broom, J. Todd Roach, H. Ranjith W. Dharmaratne, N.p. Dhammika Nanayakkara, Ikhlas A. Khan, Kenneth J. Sufka
    Abstract:

    Rationale: Piper methysticum extract (kava kava) possesses numerous therapeutic properties, but it is unknown which of its principle constituents (kavalactones) subserve such effects. Objectives: This experiment sought to characterize the putative anxiolytic properties of P. methysticum extract and its six principle kavalactones in the chick social separation-stress paradigm. Methods: Eight-day-old chicks received intraperitoneal injections of either vehicle, chlordiazepoxide (5.0 mg/ml per kg), P. methysticum extract (containing 30% kavalactones), kavain, Dihydrokavain, methysticin, dihydromethysticin, yangonin, or desmethoxyyangonin (30 mg/ml per kg for kava compounds) 30 min prior to being tested in the presence of two conspecifics or in isolation for a 3-min observation period. Latency to adopt a ventral recumbent posture to index sedation, number of vocalizations to index separation distress, and a composite pain score (in response to 50 µl 0.10% formalin injection into the plantar surface of the foot) to index stress-induced analgesia served as dependent measures. Results: Both chlordiazepoxide and P. methysticum extract attenuated separation-induced distress vocalizations and stress-induced analgesia. Dihydrokavain attenuated separation-induced distress vocalizations. Conclusions: These findings suggest that the anxiolytic effects of P. methysticum extract may be mediated, in part, by Dihydrokavain.

Xiaoming Feng - One of the best experts on this subject based on the ideXlab platform.

Pramod Upadhyaya - One of the best experts on this subject based on the ideXlab platform.

  • Pilot in Vivo Structure–Activity Relationship of Dihydromethysticin in Blocking 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone-Induced O6-Methylguanine and Lung Tumor in A/J Mice
    Journal of Medicinal Chemistry, 2017
    Co-Authors: Manohar Puppala, Sreekanth C Narayanapillai, Pablo Leitzman, M. Gerard O'sullivan, Stephen S. Hecht, Pramod Upadhyaya, Chengguo Xing
    Abstract:

    (+)-Dihydromethysticin was recently identified as a promising lung cancer chemopreventive agent, while (+)-Dihydrokavain was completely ineffective. A pilot in vivo structure–activity relationship (SAR) was explored, evaluating the efficacy of its analogs in blocking 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced short-term O6-methylguanine and long-term adenoma formation in the lung tissues in A/J mice. Both results revealed cohesive SARs, demonstrating that the methylenedioxy functional group in DHM is essential while the lactone functional group tolerates modifications.

  • Pilot in Vivo Structure–Activity Relationship of Dihydromethysticin in Blocking 4‑(Methylnitrosamino)-1-(3-pyridyl)-1-butanone-Induced O6‑Methylguanine and Lung Tumor in A/J Mice
    2017
    Co-Authors: Manohar Puppala, Sreekanth C Narayanapillai, Pablo Leitzman, Stephen S. Hecht, Pramod Upadhyaya, Haifeng Sun, Gerard M. O’sullivan, Chengguo Xing
    Abstract:

    (+)-Dihydromethysticin was recently identified as a promising lung cancer chemopreventive agent, while (+)-Dihydrokavain was completely ineffective. A pilot in vivo structure–activity relationship (SAR) was explored, evaluating the efficacy of its analogs in blocking 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced short-term O6-methylguanine and long-term adenoma formation in the lung tissues in A/J mice. Both results revealed cohesive SARs, demonstrating that the methylenedioxy functional group in DHM is essential while the lactone functional group tolerates modifications

  • dihydromethysticin dhm blocks tobacco carcinogen 4 methylnitrosamino 1 3 pyridyl 1 butanone nnk induced o6 methylguanine in a manner independent of the aryl hydrocarbon receptor ahr pathway in c57bl 6 female mice
    Chemical Research in Toxicology, 2016
    Co-Authors: Sreekanth C Narayanapillai, Pablo Leitzman, Chengguo Xing, Carolyn J Baglole, Pramod Upadhyaya
    Abstract:

    4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a key carcinogen responsible for tobacco smoke-induced lung carcinogenesis. Among the types of DNA damage caused by NNK and its metabolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), O6-methylguanine (O6-mG) is likely the most carcinogen in A/J mice. Results of our previous studies showed that levels of O6-mG and other types of NNAL-derived DNA damage were preferentially reduced in the lung of female A/J mice upon dietary treatment with dihydromethysticin (DHM), a promising lung cancer chemopreventive agent from kava. Such a differential blockage may be mediated via an increased level of NNAL glucuronidation, thereby leading to its detoxification. The potential of the aryl hydrocarbon receptor (AhR) as an upstream target of DHM mediating these events was evaluated herein using Ahr+/– and Ahr–/– C57BL/6 female mice because DHM was reported as an AhR agonist. DHM (0.05, 0.2, and 1.0 mg/g of diet) and Dihydrokavain (DHK, an inactive analogue,...

  • dihydromethysticin from kava blocks tobacco carcinogen 4 methylnitrosamino 1 3 pyridyl 1 butanone induced lung tumorigenesis and differentially reduces dna damage in a j mice
    Carcinogenesis, 2014
    Co-Authors: Sreekanth C Narayanapillai, Pablo Leitzman, Ahmad Ali Shaik, Gerard M Osullivan, Alex E. Grill, Silvia Balbo, Lisa A Peterson, Pramod Upadhyaya, Bo Zhou, Junxuan Lu
    Abstract:

    We have previously shown that kava and its flavokavain-free Fraction B completely blocked 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice with a preferential reduction in NNK-induced O 6-methylguanine (O 6-mG). In this study, we first identified natural (+)-dihydromethysticin (DHM) as a lead compound through evaluating the in vivo efficacy of five major compounds in Fraction B on reducing O 6-mG in lung tissues. (+)-DHM demonstrated outstanding chemopreventive activity against NNK-induced lung tumorigenesis in A/J mice with 97% reduction of adenoma multiplicity at a dose of 0.05mg/g of diet (50 ppm). Synthetic (±)-DHM was equally effective as the natural (+)-DHM in these bioassays while a structurally similar analog, (+)-Dihydrokavain (DHK), was completely inactive, revealing a sharp in vivo structure–activity relationship. Analyses of an expanded panel of NNK-induced DNA adducts revealed that DHM reduced a subset of DNA adducts in lung tissues derived from 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL, the active metabolite of NNK). Preliminary 17-week safety studies of DHM in A/J mice at a dose of 0.5mg/g of diet (at least 10× its minimum effective dose) revealed no adverse effects, suggesting that DHM is likely free of kava’s hepatotoxic risk. These results demonstrate the outstanding efficacy and promising safety margin of DHM in preventing NNK-induced lung tumorigenesis in A/J mice, with a unique mechanism of action and high target specificity.