Protection against hepatic ischemia-reperfusion injury in rats by oral pretreatment with quercetin.
OBJECTIVE
To investigate the possible protection provided by oral quercetin pretreatment against hepatic ischemia-reperfusion injury in rats.


METHODS
The 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.


RESULTS
Hepatic 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.


CONCLUSIONS
It 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.
Su
Jun-Feng
JF
Department of Nutrition, Institute of Hygiene and Environmental Medicine, Tianjin 300050, China.
Guo
Chang-Jiang
CJ
Wei
Jing-Yu
JY
Yang
Ji-Jun
JJ
Jiang
Yu-Gang
YG
Li
Yun-Feng
YF
D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000493:pharmacokinetics / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000493:pharmacokinetics / Q000627:therapeutic use; D001682:Biological Availability; D015415:Biomarkers / Q000097:blood; D053938:DNA Fragmentation; D005979:Glutathione Peroxidase / Q000378:metabolism; D008099:Liver / Q000098:blood supply / Q000187:drug effects* / Q000201:enzymology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D011794:Quercetin / Q000493:pharmacokinetics / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000097:blood / Q000201:enzymology / Q000378:metabolism / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism; D000637:Transaminases / Q000097:blood; D014969:Xanthine Oxidase / Q000378:metabolism
D000975:Antioxidants; D015415:Biomarkers; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D011794:Quercetin; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase; D000637:Transaminases; D001205:Ascorbic Acid