Simple jQuery Dropdowns
Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/17132
Title: Hepatotoxic effect of barakol in mice
Authors: Watcharaporn Devakul Na Ayutthaya
Pornpen Pramyothin
Pawinee Piyachaturawat
Wichai Ekataksin
Pranee Chavalittumrong
Songphol Chivapat
Chaiyo Chaichantipyuth
Chulalongkorn University
Mahidol University
Thailand Ministry of Public Health
Keywords: Medicine;Pharmacology, Toxicology and Pharmaceutics
Issue Date: 1-Jan-2005
Citation: Journal of Traditional Medicines. Vol.22, No.1 (2005), 9-14
Abstract: Acute and subacute hepatotoxicity induced by barakol was investigated in mice. Blood clinical biochemistry parameters (serum AST, ALT, total bilirubin, cholesterol, triglyceride and glucose) and histopathological examination were used as criteria for liver injury. Mice were given barakol in a single dose (100, 200, 300 and 400 mg/kg, p.o.) and repeated doses (100, 200 and 300 mg/kg/day, p.o., 28 days) for acute and subacute toxicity studies, respectively. The acute and subacute hepatotoxic findings included the increase in total bilirubin, AST and ALT levels and the decrease in cholesterol, triglyceride and glucose concentrations which corresponded to the histopathological examination showing the hydropic swelling of hepatocytes, scattered degree of necrotic cells around central vein spreading to periportal zone and finally apoptotic cell death around centrilobular zone spreading to periportal area. The degree of the severity of barakol induced liver injury was dose and time dependent. The mechanism involved may be the induction of necrosis and apoptosis, resulting in the disturbance of normal liver cell function. The ultimate outcome of hepatotoxicity by barakol depended on the balance between the extent of liver cell damage and its repair. There were signs of liver regeneration and recovery in all doses of barakol treatment. Reduction of total cytochrome P450 content with unchanged protein expression of CYP 3A1 and 2E1, inhibition of mitochondrial respiration and hemolysis of red blood cells may be involved in barakol induced hepatotoxicity. © 2005, Medical and Pharmaceutical Society for WAKAN-YAKU. All rights reserved.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=80052022126&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/17132
ISSN: 18813747
18801447
Appears in Collections:Scopus 2001-2005

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.