Article Publish Status: FREE
Abstract Title:

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

Abstract Source:

Oncotarget. 2017 Sep 15 ;8(40):68668-68674. Epub 2017 Aug 2. PMID: 28978146

Abstract Author(s):

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

Article Affiliation:

Guanghong Xie


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.

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