Protection against hepatic ischemia-reperfusion injury in rats by oral pretreatment with quercetin.
- Author:
Jun-Feng SU
1
;
Chang-Jiang GUO
;
Jing-Yu WEI
;
Ji-Jun YANG
;
Yu-Gang JIANG
;
Yun-Feng LI
Author Information
- Publication Type:Journal Article
- MeSH: Administration, Oral; Animals; Antioxidants; pharmacokinetics; therapeutic use; Ascorbic Acid; pharmacokinetics; therapeutic use; Biological Availability; Biomarkers; blood; DNA Fragmentation; Glutathione Peroxidase; metabolism; Liver; blood supply; drug effects; enzymology; Male; Malondialdehyde; blood; Quercetin; pharmacokinetics; therapeutic use; Rats; Rats, Wistar; Reactive Oxygen Species; metabolism; Reperfusion Injury; blood; enzymology; metabolism; prevention & control; Superoxide Dismutase; metabolism; Transaminases; blood; Xanthine Oxidase; metabolism
- From: Biomedical and Environmental Sciences 2003;16(1):1-8
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the possible protection provided by oral quercetin pretreatment against hepatic ischemia-reperfusion injury in rats.
METHODSThe quercetin (0.13 mmol/kg) was orally administrated in 50 min prior to hepatic ischemia-reperfusion injury. Ascorbic acid was also similarly administered. The hepatic content of quercetin was assayed by high performance liquid chromatography (HPLC). Plasma glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT) activities and malondialdehyde (MDA) concentration were measured as markers of hepatic ischemia-reperfusion injury. Meanwhile, hepatic content of glutathione (GSH), activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and xanthine oxidase (XO), total antioxidant capacity (TAOC), contents of reactive oxygen species (ROS) and MDA, DNA fragmentation were also determined.
RESULTSHepatic content of quercetin after intragastric administration of quercetin was increased significantly. The increases in plasma GPT, GOT activities and MDA concentration after hepatic ischemia-reperfusion injury were reduced significantly by pretreatment with quercetin. Hepatic content of GSH and activities of SOD, GSH-Px and TAOC were restored remarkably while the ROS and MDA contents were significantly diminished by quercetin pretreatment after ischemia-reperfusion injury. However, quercetin pretreatment did not reduce significantly hepatic XO activity and DNA fragmentation. Ascorbic acid pretreatment had also protective effects against hepatic ischemia-reperfusion injury by restoring hepatic content of GSH, TAOC and diminishing ROS and MDA formation and DNA fragmentation.
CONCLUSIONIt is indicated that quercetin can protect the liver against ischemia-reperfusion injury after oral pretreatment and the underlying mechanism is associated with improved hepatic antioxidant capacity.