Hepatoprotective effect of Artemisia Argyi essential oil on bisphenol A‐induced hepatotoxicity via inhibition of ferroptosis in mice

Author:

Cui Weiqi1,Zhou Hui1,Zhang Jingxian1,Zhang Junwei1,Wu Deqiao1,Rong Ying1,Liu Fanglin1,Liu Junhui1,Liu Haiyan1,Wei Bo1,Tang Youcai2,Liao Xinglin3,Xu Xia1ORCID

Affiliation:

1. Key Laboratory of Advanced Drug Preparation Technologies, Ministry of Education of China; School of Pharmaceutical Sciences Zhengzhou University Zhengzhou China

2. Henan Joint International Research Laboratory of Chronic Liver Injury, Henan Key Laboratory of Rehabilitation Medicine, Department of Pediatrics, the Fifth Affiliated Hospital Zhengzhou University Zhengzhou China

3. Nanyang Lanhaisenyuan Medical Technology Ltd, Co Nanyang China

Abstract

AbstractThe environmental pollutant bisphenol A (BPA), used in the manufacture of plastic packaging materials for various diets, is widely distributed in the environment and causes severe hepatotoxicity by inducing oxidative stress. Artemisia argyi essential oil (AAEO), a volatile oil component isolated from Artemisia argyi H.Lév. & Vaniot, has pharmacological effects, especially for hepatoprotective actions. However, the potential effect of AAEO in BPA induced hepatotoxicity has not been characterized. First, we analyzed the chemical composition in AAEO by gas chromatography–mass spectrometry. Herein, we investigated the effect of AAEO on hepatic metabolic changes in mice exposed to BPA. Results showed that compared with the BPA group, AAEO could reduce the level of liver function enzymes in BPA mice serum, and ameliorate hepatic lesions and fibrosis. Additionally, 20 differential metabolites screened by metabolomics were mainly involved in the reprogramming of glutathione metabolism, purine metabolism, and polyunsaturated fatty acid synthesis. Moreover, AAEO could reduce hepatic ferroptosis induced by BPA, as demonstrated by reducing xanthine oxidase activity, up‐regulating the activities of glutathione peroxidase 4 (GPX4), superoxide dismutase, and catalase and the expression of SLC7A11 to promote the glutathione synthetic, while inhibiting transferrin receptor 1 (TFR1) expression to reduce the accumulation of Fe2+ in cells. Therefore, our study identified AAEO as a hepatic protectant against BPA‐induced hepatotoxicity by reversing the occurrence of ferroptosis.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Management, Monitoring, Policy and Law,Toxicology,General Medicine

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