Oligonol Ameliorates CCl4-Induced Liver Injury in Rats via the NF-Kappa B and MAPK Signaling Pathways. (21st December 2015)

• Record Type: Journal Article
• Authors: Bak, Jeonghyeon; Je, Nam Kyung; Chung, Hae Young; Yokozawa, Takako; Yoon, Sik; Moon, Jeon-Ok
• Other Names: Muriel Pablo Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2016(2016)
• Publication Date: 2015-12-21
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2016/3935841
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : Oxidative stress is thought to be a key risk factor in the development of hepatic diseases. Blocking or retarding the reactions of oxidation and the inflammatory process by antioxidants could be a promising therapeutic intervention for prevention or treatment of liver injuries. Oligonol is a low molecular weight polyphenol containing catechin-type monomers and oligomers derived from lychee fruit. In this study, we investigated the anti-inflammatory effect of oligonol on carbon tetrachloride- (CCl4 -) induced acute hepatic injury in rats. Oral administration of oligonol (10 or 50 mg/kg) reduced CCl4 -induced abnormalities in liver histology and serum AST and serum ALT levels. Oligonol treatment attenuated the CCl4 -induced production of inflammatory mediators, including TNF- α, IL-1 β, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) mRNA levels. Western blot analysis showed that oligonol suppressed proinflammatory nuclear factor-kappa B (NF- κ B) p65 activation, phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun NH2 -terminal kinase (JNK), and p38 mitogen-activated protein kinases (MAPKs) as well as Akt. Oligonol exhibited strong antioxidative activity in vitro and in vivo, and hepatoprotective activity against t -butyl hydroperoxide-induced HepG2 cells. Taken together, oligonol showed antioxidative and anti-inflammatory effects in CCl4 -intoxicated rats by inhibiting oxidative stress and NF- κ B activation via blockade of the activation of upstream kinases including MAPKs and Akt.