Beneficial Effects of Quercetin on Ischemia/Reperfusion-Induced Liver Injury in an Animal Model

Authors

  • Toru Shizuma Department of Physiology, Tokai University School of Medicine, 143, Shimokasuya, Isehara, Kanagawa 259-1193, Japan.

DOI:

https://doi.org/10.9734/bpi/acmmr/v7/6821B

Keywords:

Ischemia/reperfusion-induced liver injury, quercetin, oxidative and nitrogen stress, antioxidative effects, nitrotyrosine

Abstract

Background: Ischemia/reperfusion (I/R)-induced liver injury, which may lead to organ failure, is a major complication of hepatic surgery. I/R-induced liver injury is exacerbated by oxidative and nitrogen stress. Although quercetin, a plant-derived flavonoid, is a potent antioxidant, only a few studies focused on the effects of quercetin on I/R-induced liver injury.
Aim of Study: In this study, the effects of quercetin were examined in an animal model of I/R-induced liver injury.
Methods: F344 rats were divided into a negative control group and a group treated with intraperitoneal administration of quercetin (100 mg/kg). In both groups, the portal vein was ligated for 60 min to induce ischemia. Blood was collected after 60 min of reperfusion. Serum transaminase levels, tumor necrosis factor (TNF)-\(\alpha\) levels, and blood nitrotyrosine levels were measured. Livers were excised for histological examination.
Results and Conclusion: Serum transaminases, TNF-\(\alpha\), and nitrotyrosine levels were significantly lower in the quercetin-treated group compared with the levels in the negative control group. Liver damage was reduced in the quercetin-treated group compared with the negative control group. These results suggest that quercetin may attenuate the effects of I/R injury via antioxidative effects that inhibit proinflammatory cytokine production.

Published

2023-12-07

How to Cite

Toru Shizuma. (2023). Beneficial Effects of Quercetin on Ischemia/Reperfusion-Induced Liver Injury in an Animal Model . Advanced Concepts in Medicine and Medical Research Vol. 7, 1–9. https://doi.org/10.9734/bpi/acmmr/v7/6821B