4.7 Article

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

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FRONTIERS IN PHARMACOLOGY
卷 12, 期 -, 页码 -

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FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2021.586010

关键词

quercitrin; acute liver injury; acetaminophen; complex I; mitochondrial dysfunction; reactive oxygen species

资金

  1. National Natural Science Foundation of China [31570343]
  2. Key Laboratory of Traditional Chinese Medicine Resources and Chemistry of Hubei Province, Hubei University of Chinese Medicine, Wuhan, Hubei, China

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The flavonoid quercitrin has a protective effect on the liver by attenuating acetaminophen-induced acute liver injury, restoring mitochondrial function, reducing oxidative stress, and maintaining mitochondrial complex I levels. The study provides insights into the potential therapeutic mechanism of quercitrin.
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 in vivo 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 alpha (TNF-alpha), 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 in vitro 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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