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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- (CCl 4 -) induced acute hepatic injury in rats. Oral administration of oligonol (10 or 50 mg/kg) reduced CCl 4 -induced abnormalities in liver histology and serum AST and serum ALT levels. Oligonol treatment attenuated the CCl 4 -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 NH 2 -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 CCl 4 -intoxicated rats by inhibiting oxidative stress and NF- κ B activation via blockade of the activation of upstream kinases including MAPKs and Akt.

Oligonol Ameliorates CCl4-Induced Liver Injury in Rats via the NF-Kappa B and MAPK Signaling Pathways

Oligonol Ameliorates CCl₄-Induced Liver Injury in Rats via the NF-Kappa B and MAPK Signaling Pathways