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Effects of β-eudesmol and atractylodin on target genes and hormone related to cardiotoxicity, hepatotoxicity, and endocrine disruption in developing zebrafish embryos
Atractylodes lancea, commonly known as Kod-Kamao in Thai, a traditional medicinal herb, is being developed for clinical use in cholangiocarcinoma. β-eudesmol and atractylodin are the main active components of this herb which possess most of the pharmacological properties. However, the lack of adequa...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10306152/ https://www.ncbi.nlm.nih.gov/pubmed/36474426 http://dx.doi.org/10.1177/00368504221137458 |
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author | Tshering, Gyem Pimtong, Wittaya Plengsuriyakarn, Tullayakorn Na-Bangchang, Kesara |
author_facet | Tshering, Gyem Pimtong, Wittaya Plengsuriyakarn, Tullayakorn Na-Bangchang, Kesara |
author_sort | Tshering, Gyem |
collection | PubMed |
description | Atractylodes lancea, commonly known as Kod-Kamao in Thai, a traditional medicinal herb, is being developed for clinical use in cholangiocarcinoma. β-eudesmol and atractylodin are the main active components of this herb which possess most of the pharmacological properties. However, the lack of adequate toxicity data would be a significant hindrance to their further development. The present study investigated the toxic effects of selected concentrations of β-eudesmol and atractylodin in the heart, liver, and endocrine systems of zebrafish embryos. Study endpoints included changes in the expression of genes related to Na/K-ATPase activity in the heart, fatty acid-binding protein 10a and cytochrome P450 family 1 subfamily A member 1 in the liver, and cortisol levels in the endocrine system. Both compounds produced inhibitory effects on the Na/K-ATPase gene expressions in the heart. Both also triggered the biomarkers of liver toxicity. While β-eudesmol did not alter the expression of the cytochrome P450 family 1 subfamily A member 1 gene, atractylodin at high concentrations upregulated the gene, suggesting its potential enzyme-inducing activity in this gene. β-eudesmol, but not atractylodin, showed some stress-reducing properties with suppression of cortisol production. |
format | Online Article Text |
id | pubmed-10306152 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-103061522023-08-09 Effects of β-eudesmol and atractylodin on target genes and hormone related to cardiotoxicity, hepatotoxicity, and endocrine disruption in developing zebrafish embryos Tshering, Gyem Pimtong, Wittaya Plengsuriyakarn, Tullayakorn Na-Bangchang, Kesara Sci Prog Original Article Atractylodes lancea, commonly known as Kod-Kamao in Thai, a traditional medicinal herb, is being developed for clinical use in cholangiocarcinoma. β-eudesmol and atractylodin are the main active components of this herb which possess most of the pharmacological properties. However, the lack of adequate toxicity data would be a significant hindrance to their further development. The present study investigated the toxic effects of selected concentrations of β-eudesmol and atractylodin in the heart, liver, and endocrine systems of zebrafish embryos. Study endpoints included changes in the expression of genes related to Na/K-ATPase activity in the heart, fatty acid-binding protein 10a and cytochrome P450 family 1 subfamily A member 1 in the liver, and cortisol levels in the endocrine system. Both compounds produced inhibitory effects on the Na/K-ATPase gene expressions in the heart. Both also triggered the biomarkers of liver toxicity. While β-eudesmol did not alter the expression of the cytochrome P450 family 1 subfamily A member 1 gene, atractylodin at high concentrations upregulated the gene, suggesting its potential enzyme-inducing activity in this gene. β-eudesmol, but not atractylodin, showed some stress-reducing properties with suppression of cortisol production. SAGE Publications 2022-12-06 /pmc/articles/PMC10306152/ /pubmed/36474426 http://dx.doi.org/10.1177/00368504221137458 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Article Tshering, Gyem Pimtong, Wittaya Plengsuriyakarn, Tullayakorn Na-Bangchang, Kesara Effects of β-eudesmol and atractylodin on target genes and hormone related to cardiotoxicity, hepatotoxicity, and endocrine disruption in developing zebrafish embryos |
title | Effects of β-eudesmol and atractylodin on target genes and hormone
related to cardiotoxicity, hepatotoxicity, and endocrine disruption in
developing zebrafish embryos |
title_full | Effects of β-eudesmol and atractylodin on target genes and hormone
related to cardiotoxicity, hepatotoxicity, and endocrine disruption in
developing zebrafish embryos |
title_fullStr | Effects of β-eudesmol and atractylodin on target genes and hormone
related to cardiotoxicity, hepatotoxicity, and endocrine disruption in
developing zebrafish embryos |
title_full_unstemmed | Effects of β-eudesmol and atractylodin on target genes and hormone
related to cardiotoxicity, hepatotoxicity, and endocrine disruption in
developing zebrafish embryos |
title_short | Effects of β-eudesmol and atractylodin on target genes and hormone
related to cardiotoxicity, hepatotoxicity, and endocrine disruption in
developing zebrafish embryos |
title_sort | effects of β-eudesmol and atractylodin on target genes and hormone
related to cardiotoxicity, hepatotoxicity, and endocrine disruption in
developing zebrafish embryos |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10306152/ https://www.ncbi.nlm.nih.gov/pubmed/36474426 http://dx.doi.org/10.1177/00368504221137458 |
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