Document Detail


Co-administration of C-Phycocyanin ameliorates thioacetamide-induced hepatic encephalopathy in Wistar rats.
MedLine Citation:
PMID:  17169376     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fulminant hepatic failure (FHF) is a condition with a sudden onset of necrosis followed by degeneration of hepatocytes, without any previously established liver disease, generally occurring within hours or days. FHF is associated with a wide spectrum of neuropsychiatric alterations ranging from stupor to coma, culminating in death. In the present study FHF was induced in rats by the administration of thioacetamide (TAA). Oxidative stress is thought to play a prominent role in the pathophysiology of cerebral changes during FHF leading to the assumption that antioxidants might offer protection. Hence, in the present study the protective effect of C-Phycocyanin (C-PC), a natural antioxidant, was evaluated on TAA-induced tissue damage. C-Phycocyanin was administered intraperitoneally twice at 24 h interval (50 mg/kg body weight) along with the hepatotoxin TAA (300 mg/kg body weight). The animals were sacrificed 18 h after the second injection of TAA treatment and various biochemical parameters were analysed in liver, serum and brain tissues. These studies revealed significant prevention of TAA-induced liver damage by C-PC, as evidenced by a) increase in survival rate; b) the prevention of leakage of liver enzymes (AAT and AST) and ammonia into serum; c) increase in prothrombin time and d) liver histopathology. Ultrastructural studies of astrocytes of different regions of brain clearly showed a decrease in edema after C-PC treatment. TAA-induced histopathological lesions in different regions of the brain namely cerebral cortex, cerebellum and pons medulla were significantly reduced by the co-administration of C-PC with TAA. Further C-PC treatment resulted in a) decrease in the levels of tryptophan and markers of lipid peroxidation and b) elevation in the activity levels of catalase, glutathione peroxidase in different regions of brain. These studies reveal the potential of C-PC in ameliorating TAA-induced hepatic encephalopathy by improving antioxidant defenses.
Authors:
K V Sathyasaikumar; I Swapna; P V B Reddy; Ch R K Murthy; K R Roy; A Dutta Gupta; B Senthilkumaran; P Reddanna
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Publication Detail:
Type:  Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-12-12
Journal Detail:
Title:  Journal of the neurological sciences     Volume:  252     ISSN:  0022-510X     ISO Abbreviation:  J. Neurol. Sci.     Publication Date:  2007 Jan 
Date Detail:
Created Date:  2006-12-20     Completed Date:  2007-03-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375403     Medline TA:  J Neurol Sci     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  67-75     Citation Subset:  IM    
Affiliation:
Department of Animal Sciences, School of Life Sciences, University of Hyderabad, Hyderabad-500 046, India.
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MeSH Terms
Descriptor/Qualifier:
Albumins / metabolism
Ammonia / metabolism
Animals
Antioxidants / administration & dosage*
Brain / drug effects,  metabolism,  ultrastructure
Dose-Response Relationship, Drug
Drug Interactions
Hepatic Encephalopathy / chemically induced,  mortality,  pathology,  prevention & control*
Lipid Peroxidation / drug effects
Liver / drug effects,  metabolism
Male
Microscopy, Electron, Transmission / methods
Phycocyanin / administration & dosage*
Rats
Rats, Wistar
Reaction Time / drug effects
Survival Rate
Thioacetamide*
Tryptophan / metabolism
Chemical
Reg. No./Substance:
0/Albumins; 0/Antioxidants; 11016-15-2/Phycocyanin; 62-55-5/Thioacetamide; 73-22-3/Tryptophan; 7664-41-7/Ammonia

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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