Protective effect of baicalin against carbon tetrachloride-induced acute hepatic injury in mice.
This study examined the effects of baicalin, a bioactive flavonoid isolated from Scutellariae Radix, on carbon tetrachloride (CCl(4))-induced liver injury. Mice were treated intraperitoneally with 0.5 ml/kg CCl(4) and different groups of animals received 25, 50, 100, and 200 mg/kg baicalin. At 24 h after the CCl(4) treatment, the level of serum aminotransferases and lipid peroxidation was significantly elevated, whereas the hepatic glutathione content was decreased. These changes were attenuated by baicalin. The histological studies showed that baicalin inhibited the portal inflammation, centrizonal necrosis, and Kupffer cell hyperplasia, which are the three most common characteristics of CCl(4)-induced liver damage. The serum level and mRNA expression of tumor necrosis factor-alpha were markedly increased by the CCl(4) treatment but suppressed by baicalin. The mRNA and protein expression levels of inducible nitric oxide synthase and heme oxygenase-1 increased significantly at 24 h after the CCl(4) treatment. Baicalin attenuated the increase in the protein and gene expression of inducible nitric oxide synthase but augmented the increase in those of heme oxygenase-1. These findings suggest that baicalin protects hepatocytes from the oxidative damage caused by CCl(4), and this protection is likely due to the induction of HO-1 expression and the inhibition of the proinflammatory mediators.
Park
Sang-Won
SW
College of Pharmacy, Sungkyunkwan University, Jangan-gu, Suwon-si, Gyeonggi-do, Korea.
Lee
Chan-Ho
CH
Kim
Yeong Shik
YS
Kang
Sam Sik
SS
Jeon
Su Jin
SJ
Son
Kun Ho
KH
Lee
Sun-Mee
SM
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D002251:Carbon Tetrachloride; D056486:Chemical and Drug Induced Liver Injury; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005419:Flavonoids / Q000494:pharmacology* / Q000627:therapeutic use; D005978:Glutathione / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008107:Liver Diseases / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008813:Mice, Inbred ICR; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D012333:RNA, Messenger / Q000378:metabolism; D013997:Time Factors; D000637:Transaminases / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics
D000975:Antioxidants; D005419:Flavonoids; D008565:Membrane Proteins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C038044:baicalin; D002251:Carbon Tetrachloride; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D051547:Heme Oxygenase-1; C496542:Hmox1 protein, mouse; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D000637:Transaminases; D005978:Glutathione