Protective effects of hyperoside against carbon tetrachloride-induced liver damage in mice

Choi, JH; Kim, DW; Yun, N; Choi, JS; Islam, MN; Kim, YS; Lee, SM

HERO ID

874811

Reference Type

Journal Article

Year

2011

Language

English

PMID

21428416

HERO ID 874811
In Press No
Year 2011
Title Protective effects of hyperoside against carbon tetrachloride-induced liver damage in mice
Authors Choi, JH; Kim, DW; Yun, N; Choi, JS; Islam, MN; Kim, YS; Lee, SM
Journal Journal of Natural Products
Volume 74
Issue 5
Page Numbers 1055-1060
Abstract In this study, the hepatoprotective effects of hyperoside (1), a flavonoid glycoside isolated from Artemisia capillaris, have been examined against carbon tetrachloride (CCl4)-induced liver injury. Mice were treated intraperitoneally with vehicle or 1 (50, 100, and 200 mg·kg(-1)) 30 min before and 2 h after CCl4 (20 μL·kg(-1)) injection. Levels of serum aminotransferases were increased 24 h after CCl4 injection, and these increases were attenuated by 1. Histological analysis showed that 1 prevented portal inflammation, centrizonal necrosis, and Kupffer cell hyperplasia. Lipid peroxidation was increased and hepatic glutathione content was decreased significantly after CCl4 treatment, and these changes were reduced by administration of 1. Protein and mRNA expression of tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and heme oxygenase-1 (HO-1) and nuclear protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2) significantly increased after CCl4 injection. Compound 1 suppressed TNF-α, iNOS, and COX-2 protein and mRNA expression and augmented HO-1 protein and mRNA expression and Nrf2 nuclear protein expression. These results suggest that 1 has protective effects against CCl4-induced acute liver injury, and this protection is likely due to enhancement of the antioxidative defense system and suppression of the inflammatory response.
Doi 10.1021/np200001x
Pmid 21428416
Wosid WOS:000291127900021
Is Certified Translation No
Dupe Override No
Comments Source: Web of Science WOS:000291127900021
Is Public Yes
Language Text English
Is Qa No