Aristolochic acid-induced dyslipidemia and hepatotoxicity: The potential role of FXR and AHR receptors

Aristolochic acids (AAs) represent a class of nitrophenanthrene carboxylic acids naturally existing or accidentally mixed in herbal medicines or crops, which have long been recognized for causing nephropathy. Recently, the linkage between AAs and liver injury has become a concern; however, the curre...

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Main Authors: Yumei Ma, Chenlong Du, Yuzhen Liu, Meiyao Feng, Yingqing Shou, Dianke Yu, Yuan Jin
Format: Article
Language:English
Published: Elsevier 2024-11-01
Series:Ecotoxicology and Environmental Safety
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Online Access:http://www.sciencedirect.com/science/article/pii/S0147651324013423
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author Yumei Ma
Chenlong Du
Yuzhen Liu
Meiyao Feng
Yingqing Shou
Dianke Yu
Yuan Jin
author_facet Yumei Ma
Chenlong Du
Yuzhen Liu
Meiyao Feng
Yingqing Shou
Dianke Yu
Yuan Jin
author_sort Yumei Ma
collection DOAJ
description Aristolochic acids (AAs) represent a class of nitrophenanthrene carboxylic acids naturally existing or accidentally mixed in herbal medicines or crops, which have long been recognized for causing nephropathy. Recently, the linkage between AAs and liver injury has become a concern; however, the current understanding of the mechanism or mode of action (MOA) is limited. In the present study, we investigated nuclear receptor-mediated MOA associated with AAs-induced liver injury including dyslipidemia and hepatotoxicity. Bioinformatic analysis of AAI-interacting genes indicated nuclear receptor-mediated metabolizing pathways; Transcriptomic profiling of AAs-exposed rats with liver injury suggested FXR-, NRF2-, and AHR- mediated pathways in the injured livers of the rats. Mechanistic investigation using HepG2 cells indicated AAI-induced hepatic lipid accumulation by elevating Triglyceride (TG) through inhibition of the FXR. In addition, AAI-induced hepatocellular damage by activating the AHR pathway, which further generated ROS and activated the NRF2 pathway. Together, these results provided new clues for researchers who are interested in chemical-induced liver injury.
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publishDate 2024-11-01
publisher Elsevier
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series Ecotoxicology and Environmental Safety
spelling doaj-art-89ea05c1d0ec4dacb4d85225511c04c32024-11-21T06:01:58ZengElsevierEcotoxicology and Environmental Safety0147-65132024-11-01287117266Aristolochic acid-induced dyslipidemia and hepatotoxicity: The potential role of FXR and AHR receptorsYumei Ma0Chenlong Du1Yuzhen Liu2Meiyao Feng3Yingqing Shou4Dianke Yu5Yuan Jin6School of Public Health, Qingdao University, Qingdao, ChinaNingxia Hui Autonomous Region Center for Disease Control and Prevention, Yinchuan, ChinaGaomi Municipal Center for Disease Control and Prevention, Weifang Institute of Preventive Medicine, Weifang, ChinaDepartment of Environmental Health, Qingdao Municipal Center for Disease Control and Prevention, Qingdao Institute of Preventive Medicine, Qingdao, ChinaSchool of Public Health, Qingdao University, Qingdao, ChinaSchool of Public Health, Qingdao University, Qingdao, ChinaSchool of Public Health, Qingdao University, Qingdao, China; Correspondence to: School of Public Health, Qingdao University, 308 Ningxia Road, Qingdao, Shandong 266021, China.Aristolochic acids (AAs) represent a class of nitrophenanthrene carboxylic acids naturally existing or accidentally mixed in herbal medicines or crops, which have long been recognized for causing nephropathy. Recently, the linkage between AAs and liver injury has become a concern; however, the current understanding of the mechanism or mode of action (MOA) is limited. In the present study, we investigated nuclear receptor-mediated MOA associated with AAs-induced liver injury including dyslipidemia and hepatotoxicity. Bioinformatic analysis of AAI-interacting genes indicated nuclear receptor-mediated metabolizing pathways; Transcriptomic profiling of AAs-exposed rats with liver injury suggested FXR-, NRF2-, and AHR- mediated pathways in the injured livers of the rats. Mechanistic investigation using HepG2 cells indicated AAI-induced hepatic lipid accumulation by elevating Triglyceride (TG) through inhibition of the FXR. In addition, AAI-induced hepatocellular damage by activating the AHR pathway, which further generated ROS and activated the NRF2 pathway. Together, these results provided new clues for researchers who are interested in chemical-induced liver injury.http://www.sciencedirect.com/science/article/pii/S0147651324013423Aristolochic acidsmode of action (MOA)chemical-induced liver injury (CILI)FXRAHR
spellingShingle Yumei Ma
Chenlong Du
Yuzhen Liu
Meiyao Feng
Yingqing Shou
Dianke Yu
Yuan Jin
Aristolochic acid-induced dyslipidemia and hepatotoxicity: The potential role of FXR and AHR receptors
Ecotoxicology and Environmental Safety
Aristolochic acids
mode of action (MOA)
chemical-induced liver injury (CILI)
FXR
AHR
title Aristolochic acid-induced dyslipidemia and hepatotoxicity: The potential role of FXR and AHR receptors
title_full Aristolochic acid-induced dyslipidemia and hepatotoxicity: The potential role of FXR and AHR receptors
title_fullStr Aristolochic acid-induced dyslipidemia and hepatotoxicity: The potential role of FXR and AHR receptors
title_full_unstemmed Aristolochic acid-induced dyslipidemia and hepatotoxicity: The potential role of FXR and AHR receptors
title_short Aristolochic acid-induced dyslipidemia and hepatotoxicity: The potential role of FXR and AHR receptors
title_sort aristolochic acid induced dyslipidemia and hepatotoxicity the potential role of fxr and ahr receptors
topic Aristolochic acids
mode of action (MOA)
chemical-induced liver injury (CILI)
FXR
AHR
url http://www.sciencedirect.com/science/article/pii/S0147651324013423
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