ArticleExperimental and therapeutic medicine2015
Chenodeoxycholic acid increases the induction of CYP1A1 in HepG2 and H4IIE cells.
Article in Experimental and therapeutic medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Oleanolic acid improved intestinal immune function by activating and potentiating bile acids receptor signaling in E. coli-challenged piglets.Journal of animal science and biotechnology · 2024Article
- Review
- The zhuyu pill relieves rat cholestasis by regulating the mRNA expression of lipid and bile metabolism associated genes.Frontiers in pharmacology · 2023Article
- Effects of Diminished NADPH:cytochrome P450 Reductase in Human Hepatocytes on Lipid and Bile Acid Homeostasis.Frontiers in pharmacology · 2021Article
- Histopathological features of the proper gastric glands in FVB/N-background mice carrying constitutively-active aryl-hydrocarbon receptor.BMC gastroenterology · 2019Article
- No Gut No Gain! Enteral Bile Acid Treatment Preserves Gut Growth but Not Parenteral Nutrition-Associated Liver Injury in a Novel Extensive Short Bowel Animal Model.JPEN. Journal of parenteral and enteral nutrition · 2018Article
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Authors and funding
1 author at 1 institution in 1 country.
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Abstract
Bile acids are considered to promote carcinogenesis. Cytochrome P450 1A1 (CYP1A1) plays a critical role in the biotransformation of drugs and procarcinogens. This study aimed to investigate the ability of bile acids to modulate CYP1A1 expression. Treatment of HepG2 cells with chenodeoxycholic acid (CDCA) and Sudan III (S.III) upregulated CYP1A1 transcriptional activity in HepG2 cells and CYP1A1 mRNA expression in H4IIE cells. Pretreatment of the HepG2 and H4IIE cells with CDCA upregulated the S.III-induced CYP1A transcriptional activity and mRNA expression. The CDCA-induced enhancement of CYP1A1 was not abolished by the p38 inhibitor SB203580. However, exposure of the cells to the mitogen-activated protein kinase kinase (MEK)1/2 inhibitor PD98059 suppressed the CDCA-induced enhancement of CYP1A1. These results show the ability of CDCA to upregulate CYP1A1 transcription and expression, which may explain the hepatocarcinogenesis-inducing effect of cholestasis. The CDCA-induced upregulation of CYP1A1 most probably proceeded through MEK1/2 activation, indicating that this may be a therapeutic target to prevent the cancer-promoting effects of excessive amounts of bile acids.
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Registered trials
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