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.
Oxidative stress is a hallmark of neurodegenerative disorders and is reported to be implicated in the early stage pathogenesis of neuroinflammation. In parallel, herein we assessed the alterations in the oxidative stress balance by measuring related markers. Our data indicated that LPS induced significant reduction (p<0.01) in mid-brain tissues GSH contents and sera total antioxidant capacity (TAC) levels, while MDA level was increased significantly (p<0.01) during the 4 weeks of induction compared to mock-treated rats. We also showed that treating induced rats for 4 weeks with Cur improved the oxidative state by reducing the ROS and RNS levels as well as by maintaining high tissue GSH level compared to self-recovery rats that were left for self-healing for the same period.