الفهرس 
Involvement of Cannabinoid receptors in cerebral lesions induced by Thioacetamide
List of contentsOnly 14 pages are availabe for public view
 |  | from | 140 |  |  |
| | | from | 140 | | |
Abstract
Hepatic encephalopathy is a neuropsychiatric disorder of complex pathogenesis caused by acute or chronic liver damage. The modulatory effects of WIN55,212-2 and/or rimonabant on hepatic encephalopathy associated with fulminant hepatic failure induced in mice by thioacetamide (TAA) were investigated. Mice were divided into six groups (n=12, each); animals in the 1st group were intraperitoneally injected with the vehicle, 0.2% dimethyl sulfoxide (DMSO) in saline, to serve as the control group. The other four groups were given a single dose of TAA (300 mg/kg, i.p) and were subdivided into untreated TAA and 3 treatment groups. After 24 h from TAA intoxication, mice received a single intraperitoneal injection of WIN55,212-2 (0.1mg/kg), rimonabant (0.1 mg/kg) or a combination of both, where rimonabant injection preceded WIN55,212-2 by 20 min. WIN55,212-2 and/or rimonabant reduced TAA-induced hepatic injury as depicted by the decreased levels of serum ALT and AST, serum and cortical bilirubin and ammonia. They also repressed the inflammatory cascade depicted as ameliorations of cortical glycogen synthase kinase 3Ý (GSK-3Ý), S100 calcium-binding protein B (S100B), receptor for advanced glycation end-products (RAGE), nuclear factor kappa B (NF-mB), tumor necrosis factor-alpha (TNF-Ü), thiobarbituric acd reactive substance (TBARS) and nitric oxide (NO) contents while replenishing its non protein sulfhydrals (NPSHs) content. WIN55,212-2, rimonabant and their combination hampered TAA-induced encephalopathy by preserving BBB function and reducing inflammation, oxidative/nitroactive stress as well as GSK-3Ý, a kinase that drives both cascades