Naringin against doxorubicin‐induced hepatotoxicity in mice through reducing oxidative stress, inflammation, and apoptosis via the up‐regulation of SIRT1

Author:

Xi Yan1,Chi Zhongchao12,Tao Xufeng1,Zhai Xiaohan1,Zhao Zirui1,Ren Jiaqi1,Yang Shilei1,Dong Deshi1ORCID

Affiliation:

1. Department of Pharmacy First Affiliated Hospital of Dalian Medical University Dalian China

2. Department of Pharmacy Third People's Hospital of Dalian Dalian China

Abstract

AbstractClinical application of doxorubicin is limited because of its potential side effects. The present study examined whether naringin had protective actions on doxorubicin‐induced liver injury. Male BALB/c mice and alpha mouse liver 12 (AML‐12) cells were used in this paper. The results showed that AML‐12 cells treated with naringin significantly reduced cell injury, reactive oxygen species release and apoptosis level; Moreover, naringin notably alleviated liver injury by decreasing aspartate transaminase, alanine transaminase and malondialdehyde, and increasing superoxide dismutase, glutathione and catalase levels. Mechanism researches indicated that naringin increased the expression levels of sirtuin 1 (SIRT1), and inhibited the downstream inflammatory, apoptotic and oxidative stress signaling pathways. Further validation was obtained by knocking down SIRT1 in vitro, which proved the effects of naringin on doxorubicin‐induced liver injury. Therefore, naringin is a valuable lead compound for preventing doxorubicin‐induced liver damage by reducing oxidative stress, inflammation, and apoptosis via up‐regulation of SIRT1.

Publisher

Wiley

Subject

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

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