Abstract Title:

Curcumin inhibits NF-kappaB activation and reduces the severity of experimental steatohepatitis in mice.

Abstract Source:

Mech Ageing Dev. 2003 Dec;124(10-12):1025-34. PMID: 15582125

Abstract Author(s):

Isabelle A Leclercq, Geoffrey C Farrell, Christine Sempoux, Aileen dela Peña, Yves Horsmans

Article Affiliation:

Gastroenterology Unit, Université Catholique de Louvain (UCL), GAEN/UCL 53/79, Avenue E. Mounier, 53, B-1200 Brussels, Belgium. isabelle_leclercq@wmi.usyd.edu.au


BACKGROUND/AIMS: While oxidative stress is a feature of non-alcoholic steatohepatitis, the causal link between oxidative stress and inflammatory recruitment has yet to be demonstrated. We analysed the role of NF-kappaB redox-sensitive signalling pathway of inflammatory recruitment in experimental steatohepatitis.

METHODS: Mice were fed the methionine and choline deficient (MCD) or the control diet, with or without curcumin, an NF-kappaB inhibitor, for up to 4 weeks. Histopathology, lipoperoxides, NF-kappaB/DNA binding and expression of NF-kappaB-regulated genes were assessed.

RESULTS: MCD-fed mice developed steatohepatitis accompanied by dramatic accumulation of hepatic lipoperoxides, activation of NF-kappaB and induction of pro-inflammatory ICAM-1, COX-2, MCP-1 and CINC mRNA. Curcumin significantly reduced MCD-induced inflammation but had no effect on steatosis or on the level of hepatic lipid peroxides. Curcumin prevented the MCD-induced activation of NF-kappaB and decreased downstream induction of ICAM-1, COX-2 and MCP-1. However, it failed to reduce activation of AP-1, MAPK pathways or CINC expression.

CONCLUSIONS: Curcumin alleviates the severity of hepatic inflammation in experimental steatohepatitis induced by the MCD diet, an effect likely to be mediated via inhibition of NF-kB activation and dependent pro-inflammatory genes. The NF-kappaB pathway is one among several possible signalling pathways by which inflammation is recruited in experimental steatohepatitis.

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