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Comprehensive Evaluation of (+)-Usnic Acid-induced Cardiotoxicity in Rats by Sequential Cross-omics Analysis.

Y Yokouchi¹, M Imaoka², N Niino²

¹1 Translational Medicine and Clinical Pharmacology Department, R&D Division, Daiichi Sankyo Co., Ltd., Tokyo, Japan.

Toxicologic Pathology

|May 20, 2017

Summary

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(+)-Usnic acid (UA) causes heart damage by triggering amino acid limitation, leading to mitochondrial issues in cardiomyocytes. This study reveals amino acid limitation as the key factor in UA-induced cardiotoxicity.

Area of Science:

Toxicology
Molecular Biology
Cardiovascular Research

Background:

(+)-Usnic acid (UA) is a natural compound with known toxic effects.
Previous studies indicated UA induces mitochondrial swelling in cardiomyocytes and alters gene expression.

Purpose of the Study:

To elucidate the pathogenesis of UA-induced cardiotoxicity.
To investigate the temporal relationship between genomic, metabolomic, and histopathological changes following UA administration.

Main Methods:

Oral administration of UA to rats for 1, 4, 7, and 14 days.
Sequential histopathological, genomic, and metabolomic analyses of heart, liver, and plasma.
Toxicogenomic analysis focusing on oxidative stress, amino acid limitation, and endoplasmic reticulum stress genes.

Keywords:

amino acid limitation heart immunohistochemistry metabolomics mitochondria molecular pathology usnic acid

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Main Results:

Mitochondrial swelling of cardiomyocytes observed by day 15, preceded by genomic upregulation on days 5 and 8.
Sustained upregulation of amino acid limitation-related genes (e.g., Mthfd2) from day 5 onwards.
Temporal upregulation of oxidative stress genes on day 5; fluctuating amino acid and bile acid metabolites observed in plasma and tissues.

Conclusions:

Amino acid limitation is identified as the pivotal toxic trigger in UA-induced cardiotoxicity.
Accumulation of bile acids may indirectly affect the myocardium, warranting further investigation.