Hepato- and neuro-protective influences of biopropolis on thioacetamide-induced acute hepatic encephalopathy in rats

• Published in: Canadian journal of physiology and pharmacology Vol. 95; no. 5; pp. 539 - 547
• Main Authors: Mostafa, Rasha E, Salama, Abeer A.A, Abdel-Rahman, Rehab F, Ogaly, Hanan A
• Format: Journal Article
• Language: English
• Published: Canada NRC Research Press 01.05.2017; Canadian Science Publishing NRC Research Press
• Subjects: Acute Disease; Animals; Biological Products - pharmacology; Biological Products - therapeutic use; biopropolis; Brain - drug effects; Brain - metabolism; Brain - pathology; Care and treatment; Deoxyribonucleic acid; DNA; DNA Fragmentation - drug effects; Encephalopathy; encéphalopathie hépatique; Gene expression; Gene Expression Regulation, Enzymologic - drug effects; Hepatic encephalopathy; Hepatic Encephalopathy - drug therapy; Hepatic Encephalopathy - metabolism; Hepatic Encephalopathy - pathology; iNOS; Liver - drug effects; Liver - metabolism; Liver - pathology; Liver diseases; Liver encephalopathy; Male; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Neuropsychology; Nitric Oxide Synthase Type II - metabolism; Oxidative stress; Oxidative Stress - drug effects; Pharmacology; Physiology; Rats; Rats, Wistar; Rodents; Thioacetamide; Thioacetamide - adverse effects; thioacétamide; vitamin E; vitamine E; Egypt; thioacetamide; vitamine E; hepatic encephalopathy; vitamin E; biopropolis; encéphalopathie hépatique; iNOS; thioacétamide
• ISSN: 0008-4212; 1205-7541
• DOI: 10.1139/cjpp-2016-0433

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome that ultimately occurs as a complication of acute or chronic liver failure; accompanied by hyperammonemia. This study aimed to evaluate the potential of biopropolis as a hepato- and neuro-protective agent using thioacetamide (TAA)-induced acute HE in rats as a model. Sixty Wistar rats were divided into 5 groups: Group 1 (normal control) received only saline and paraffin oil. Group 2 (hepatotoxic control) received TAA (300 mg/kg, once). Groups 3, 4, and 5 received TAA followed by vitamin E (100 mg/kg) and biopropolis (100 and 200 mg/kg), respectively, daily for 30 days. Evidences of HE were clearly detected in TAA-hepatotoxic group including significant elevation in the serum level of ammonia, liver functions, increased oxidative stress in liver and brain, apoptotic DNA fragmentation and overexpression of iNOS gene in brain tissue. The findings for groups administered biopropolis, highlighted its efficacy as a hepato- and neuro-protectant through improving the liver functions, oxidative status and DNA fragmentation as well as suppressing the brain expression of iNOS gene. In conclusion, biopropolis, at a dose of 200 mg/kg per day protected against TAA-induced HE through its antioxidant and antiapoptotic influence; therefore, it can be used as a protective natural product.