Oncotarget

Research Papers:

Eriodictyol attenuates arsenic trioxide-induced liver injury by activation of Nrf2

Guanghong Xie _, Xiaolin Meng, Fei Wang, Yuxin Bao and Junyuan Huo

PDF  |  HTML  |  How to cite  |  Order a Reprint

Oncotarget. 2017; 8:68668-68674. https://doi.org/10.18632/oncotarget.19822

Metrics: PDF 501 views  |   HTML 802 views  |   ?  


Abstract

Guanghong Xie1,*, Xiaolin Meng1,*, Fei Wang1, Yuxin Bao1 and Junyuan Huo1

1College of Veterinary Medicine, Jilin University, Changchun 130062, China

*These authors have contributed equally to this work

Correspondence to:

Guanghong Xie, email: Xiegh@jlu.edu.cn

Keywords: eriodictyol, arsenic trioxide, liver injury, Nrf2

Received: March 29, 2017    Accepted: June 28, 2017    Published: August 02, 2017

ABSTRACT

Arsenic, a well-known human carcinogen, has been reported to induce hepatic oxidative stress and hepatic injury. Eriodictyol, a flavonoid found in citrus fruits, has been reported to have antioxidant effects. In this study, we aimed to investigate the protective effects of eriodictyol on arsenic trioxide (As2O3)-induced liver injury and to clarify the molecular mechanism. Male Wistar rats were administrated 3mg/kg As2O3 intravenous injection at days 1, 4, 5, and 7. Eriodictyol was given 1 h before or after As2O3 treatment. The results showed that eriodictyol prevented As2O3-induced liver reactive oxygen species (ROS) and malonaldehyde (MDA) levels. Eriodictyol abrogated As2O3-induced decrease of the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) activity. Eriodictyol also attenuated As2O3-induced hepatic pathological damage. In addition, eriodictyol promoted the expression of nuclear factor erythroid 2 p45 related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) up-regulated by As2O3. In conclusion, our results demonstrated that eriodictyol exhibited a protective effect on As2O3-induced liver injury and the possible mechanism is involved in activating Nrf2 signaling pathway.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 19822