الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
In the current study we developed two independent neuroinflammatory models for the central nervous system (CNS) in order to assess the molecular pathogenesis of target signaling pathways as well as the possible intervention of curcumin as neuro-therapeutic agent. Neurotoxicity was established using (LPS) or CCl4-induced liver cirrhosis and associated hepatic encephalopathy. In the first model that was developed using LPS, in consistent with previous reports our result showed that LPS has the ability to cause neuroinflammation via glial cells activation, induction of pro-inflammatory cytokines and oxidative stress. LPS administration induced significantly the production of pro-inflammatory cytokines such as (IL-1β, TNF-α), inflammatory enzymes (COX2, iNOS, BACE1) and APP.