| Literature DB >> 34855082 |
O S Bryushinina1, Yu G Zyuz'kova1, E A Yanovskaya1, N Y Abdrashitova1, G A Frelikh1, A P Lakeev1, D V Tsuran1, V V Udut1, G N Zyuz'kov2.
Abstract
We studied the role of JNK in the regulation of the metabolism of xenobiotic venlafaxine by liver cells under in vitro conditions. The inhibitory role of this protein kinase in the biotransformation of this psychotropic agent by hepatocytes was demonstrated. JNK inhibitor added to the liver homogenate containing antidepressant enhanced and accelerated the formation of the only pharmacologically active venlafaxine metabolite O-desmethylvenlafaxine in the cell suspension. The results show the promise of studying modifiers of activity of intracellular signaling molecules (in particular, mitogen-activated protein kinases) to develop a fundamentally new approach to control the transformation of xenobiotics and to create a new class of pharmaceutical, target regulators of drugs metabolism.Entities:
Keywords: JNK; P450; intracellular signal transduction; metabolism; xenobiotics
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Year: 2021 PMID: 34855082 DOI: 10.1007/s10517-021-05352-8
Source DB: PubMed Journal: Bull Exp Biol Med ISSN: 0007-4888 Impact factor: 0.804