Quercitrin Attenuates Acetaminophen-Induced Acute Liver Injury by Maintaining Mitochondrial Complex I Activity

Overview

Journal Front Pharmacol

Date 2021 May 24

PMID 34025394

Citations 6

Authors

Weichen Xiong

Zixin Yuan

Tianshun Wang

Songtao Wu

Yiyi Xiong

Yunfeng Yao

Yanfang Yang

Hezhen Wu

Affiliations

Soon will be listed here.

Abstract

The flavonoid quercitrin has a strong antioxidant property. It is also reported to have a protective effect on the liver. However, the mechanism by which it exerts a protective effect on the liver is not fully understood. The objective of this article is to confirm the protective effect of quercitrin extracted from Albiziae flos on acetaminophen (APAP)-induced liver injury and to explain its mechanism. In the study, quercitrin was administered orally to BALB/c mice at a dose of 50, 100, and 200 mg/kg for seven consecutive days. APAP (300 mg/kg) was injected intraperitoneally after a last dose of quercitrin was administered. Determination of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA) levels showed that quercitrin effectively attenuated APAP-induced acute liver injury in mice. Results of the study showed that quercitrin reduced the levels of ROS, protected mitochondria from damage, and restored the activity of mitochondrial complex I in APAP-treated L-02 cells. The addition of rotenone which is an inhibitor of complex I blocked the protective effect of quercitrin. The expression of mitochondrial complex I was also maintained by quercitrin. Our results suggest that quercitrin can maintain the level of mitochondrial complex I in injured cells and restore its activity, which reduces the production of ROS, protects the mitochondria from oxidative stress, and has a protective effect on the liver.

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