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We began analyzing https://link.springer.com/article/10.1007/s00204-014-1230-x, but it redirected us to https://link.springer.com/article/10.1007/s00204-014-1230-x. The analysis below is for the second page.

Title[redir]:
Allyl isothiocyanate (AITC) inhibits pregnane X receptor (PXR) and constitutive androstane receptor (CAR) activation and protects against acetaminophen- and amiodarone-induced cytotoxicity | Archives of Toxicology
Description:
Antagonizing the action of the pregnane X receptor (PXR) may have important clinical implications for preventing inducer–drug interactions and improving therapeutic efficacy. We identified a widely distributed isothiocyanate, allyl isothiocyanate (AITC), which acts as an effective antagonist of the nuclear receptor pregnane X receptor (PXR, NR1I2) and constitutive androstane receptor (CAR, NR1I3). HepG2 cells were used to assay reporter function, mRNA levels, and protein expression. Catalytic activities of the PXR and CAR target genes, CYP3A4 and CYP2B6, respectively, were also assessed in differentiated HepaRG cells. Protective effects of AITC on rifampin-induced cytotoxicity were observed, and transient transfection assays showed that AITC was able to effectively attenuate the agonist effects of rifampin and CITCO on human PXR and CAR activity, respectively. AITC-mediated reduction in the transcriptional activity of PXR and CAR correlated well with the suppression of CYP3A4 and CYP2B6 expression in HepG2 cells, which reflected the reduced catalytic activities of both of these genes following AITC treatment in differentiated HepaRG cells. Furthermore, AITC disrupts the co-regulations of PXR with several important co-regulators. Furthermore, the antagonist effect of AITC against PXR was found in HepaRG cells upon addition of acetaminophen (APAP) and amiodarone, indicating that AITC protects cells from drug-induced cytotoxicity. Taken together, our results show that AITC inhibits the transactivation effects of PXR and CAR and reduces the expression and function of CYP3A4 and CYP2B6. Additionally, AITC reversed the cytotoxic effects of APAP and amiodarone induced by PXR ligand. Results from this study suggest that AITC could be a powerful agent for reducing potentially dangerous interactions between transcriptional inducers of CYP enzymes and therapeutic drugs.

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Education
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🌠 Phenomenal Traffic: 5M - 10M visitors per month

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Keywords {🔍}

pubmed, article, google, scholar, cas, receptor, human, pregnane, drug, cells, pxr, central, expression, aitc, car, chen, nuclear, pharmacol, cypa, isothiocyanate, cytochrome, allyl, activation, taiwan, university, cypb, metab, mol, toxicol, wang, toxicology, lim, induction, moore, roc, medical, gene, sci, constitutive, androstane, acetaminophen, food, chem, kliewer, cancer, china, taichung, data, research, cheng,

Topics {✒️}

preventing inducer–drug interactions cassette analysis lc-ms/ms n-acetyl-p-benzoquinone imine prc-cmv-β-galactosidase vector month download article/chapter lei wan drug-induced cytotoxicity activated pregnenolone x-receptor hepatic cytochrome p450 cytochrome p450 isoforms cytochrome p450 expression constitutive androstane receptor amiodarone-induced cytotoxicity rifampin-induced cytotoxicity chao-jung chen yun-ping lim vitro large-intestinal model nuclear receptors sxr/pxr phenobarbital-responsive nuclear translocation cytochrome p450 author information authors ethanol-mediated acetaminophen hepatotoxicity cing-yu chen jih-jung chen receptor-enhanced cyp24 expression dong-zong hung rifampicin-activated human pregnane yu-hsien lin multiple cytochromes p450 drug-induced osteomalacia related subjects primary human hepatocytes cytochrome p-450 3a shih-yu chang full article pdf acetaminophen-induced hepatotoxicity ching-hao cheng wei-cheng chen privacy choices/manage cookies idiosyncratic drug hepatotoxicity receptor-mediated cyp2b6 regulation drug-metabolizing enzymes article lim xenobiotic nuclear receptor check access β-galactosidase activity instant access drug-transporting proteins antihistaminic drug terfenadine orphan human pregnane

Questions {❓}

Boelsterli UA, Lim PL (2007) Mitochondrial abnormalities—a link to idiosyncratic drug hepatotoxicity?

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         headline:Allyl isothiocyanate (AITC) inhibits pregnane X receptor (PXR) and constitutive androstane receptor (CAR) activation and protects against acetaminophen- and amiodarone-induced cytotoxicity
         description:Antagonizing the action of the pregnane X receptor (PXR) may have important clinical implications for preventing inducer–drug interactions and improving therapeutic efficacy. We identified a widely distributed isothiocyanate, allyl isothiocyanate (AITC), which acts as an effective antagonist of the nuclear receptor pregnane X receptor (PXR, NR1I2) and constitutive androstane receptor (CAR, NR1I3). HepG2 cells were used to assay reporter function, mRNA levels, and protein expression. Catalytic activities of the PXR and CAR target genes, CYP3A4 and CYP2B6, respectively, were also assessed in differentiated HepaRG cells. Protective effects of AITC on rifampin-induced cytotoxicity were observed, and transient transfection assays showed that AITC was able to effectively attenuate the agonist effects of rifampin and CITCO on human PXR and CAR activity, respectively. AITC-mediated reduction in the transcriptional activity of PXR and CAR correlated well with the suppression of CYP3A4 and CYP2B6 expression in HepG2 cells, which reflected the reduced catalytic activities of both of these genes following AITC treatment in differentiated HepaRG cells. Furthermore, AITC disrupts the co-regulations of PXR with several important co-regulators. Furthermore, the antagonist effect of AITC against PXR was found in HepaRG cells upon addition of acetaminophen (APAP) and amiodarone, indicating that AITC protects cells from drug-induced cytotoxicity. Taken together, our results show that AITC inhibits the transactivation effects of PXR and CAR and reduces the expression and function of CYP3A4 and CYP2B6. Additionally, AITC reversed the cytotoxic effects of APAP and amiodarone induced by PXR ligand. Results from this study suggest that AITC could be a powerful agent for reducing potentially dangerous interactions between transcriptional inducers of CYP enzymes and therapeutic drugs.
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            name:China Medical University
            address:
               name:Department of Pharmacy, College of Pharmacy, China Medical University, Taichung, Taiwan, ROC
               type:PostalAddress
            type:Organization
      name:Cing-Yu Chen
      affiliation:
            name:China Medical University
            address:
               name:Department of Pharmacy, College of Pharmacy, China Medical University, Taichung, Taiwan, ROC
               type:PostalAddress
            type:Organization
      name:Tsuyoshi Yokoi
      affiliation:
            name:Kanazawa University
            address:
               name:Drug Metabolism and Toxicology, Faculty of Pharmaceutical Sciences, Kanazawa University, Kanazawa, Japan
               type:PostalAddress
            type:Organization
      name:Miki Nakajima
      affiliation:
            name:Kanazawa University
            address:
               name:Drug Metabolism and Toxicology, Faculty of Pharmaceutical Sciences, Kanazawa University, Kanazawa, Japan
               type:PostalAddress
            type:Organization
      name:Chao-Jung Chen
      affiliation:
            name:China Medical University
            address:
               name:Graduate Institute of Integrated Medicine, China Medical University, Taichung, Taiwan, ROC
               type:PostalAddress
            type:Organization
            name:China Medical University Hospital
            address:
               name:Proteomics Core Laboratory, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pharmacy, College of Pharmacy, China Medical University, Taichung, Taiwan, ROC
      name:Department of Emergency, Toxicology Center, China Medical University Hospital, Taichung, Taiwan, ROC
      name:Department of Pharmacy, College of Pharmacy, China Medical University, Taichung, Taiwan, ROC
      name:Department of Pharmacy, Changhua Show Chwan Memorial Hospital, Changhua, Taiwan, ROC
      name:Department of Pharmacy, College of Pharmacy, China Medical University, Taichung, Taiwan, ROC
      name:Department of Public Health, Chung Shan Medical University, Taichung, Taiwan, ROC
      name:Department of Pharmacy, College of Pharmacy, China Medical University, Taichung, Taiwan, ROC
      name:Department of Emergency, Toxicology Center, China Medical University Hospital, Taichung, Taiwan, ROC
      name:Graduate Institute of Pharmaceutical Technology, Tajen University, Pingtung, Taiwan, ROC
      name:School of Chinese Medicine, China Medical University, Taichung, Taiwan, ROC
      name:Department of Pharmacy, College of Pharmacy, China Medical University, Taichung, Taiwan, ROC
      name:Department of Pharmacy, College of Pharmacy, China Medical University, Taichung, Taiwan, ROC
      name:Department of Pharmacy, College of Pharmacy, China Medical University, Taichung, Taiwan, ROC
      name:Drug Metabolism and Toxicology, Faculty of Pharmaceutical Sciences, Kanazawa University, Kanazawa, Japan
      name:Drug Metabolism and Toxicology, Faculty of Pharmaceutical Sciences, Kanazawa University, Kanazawa, Japan
      name:Graduate Institute of Integrated Medicine, China Medical University, Taichung, Taiwan, ROC
      name:Proteomics Core Laboratory, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC
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