Hepatoprottective potential of ether insoluble phenolic components of n-butanol fraction (EPC-BF) of flaxseed against CCI(4) – induced liver damage in rats.

January 1, 2012 Human Health and Nutrition Data 0 Comments

Hepatoprottective potential of ether insoluble phenolic components of n-butanol fraction (EPC-BF) of flaxseed against CCI(4) – induced liver damage in rats.

Year: 2012
Authors: Kasote, D.M. Badhe, Y.S. Zanwar, A.A. Hegde, M.V. Deshmukh, K.K.
Publication Name: J Pharm Bioallied Sci.
Publication Details: Volume 4; Issue 3; Pages 231 – 235.

Abstract:

To investigate the hepatoprotective potential of ether insoluble phenolic components of n-butanol fraction (EPC BF) of flaxseed against CCl(4) induced liver damage in rats. Hepatotoxicity was induced to Wistar rats by administration of 0.2percent CCl(4) in olive oil (8 mL/kg, i.p.) on the seventh day of treatment. Hepatoprotective potential of EPC BF at doses, 250 and 500 mg/kg, p.o. was assessed through biochemical and histological parameters.EPC BF and silymarin pretreated animal groups showed significantly decreased activities of Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and level of total bilirubin, elevated by CCl(4) intoxication. Hepatic lipid peroxidation elevated by CCl(4) intoxication were also found to be alleviated at almost normal level in the EPC BF and silymarin pretreated groups. Histological studies supported the biochemical findings and treatment of EPC BF at doses 250 and 500 mg/kg, p.o. was found to be effective in restoring CCl(4)  induced hepatic damage. However, EPC BF did not show dose-dependent hepatoprotective potential. EPC BF depicted maximum protection against CCl(4)  induced hepatic damage at lower dose 250 mg/kg than higher dose (500 mg/ kg). EPC BF possesses the significant hepatoprotective activity against CCl(4) induced liver damage, which could be mediated through increase in antioxidant defenses. (Authors abstract)
In India, flaxseed has been used as both food and medicine.  In some parts of India, especially south India, it has been consumed as flaxseed chutney.  Anticancer, estrogenic, antioxidant, and hepatoprotective activities have been attributed to the flaxseed lignan content.  Most of the liver diseases generally are associated with oxidative stress caused by free radicals.  Many  health beneficial effects shown by flaxseed phenolic components are associated with its antioxidant potential.  Antioxidant potential of flaxseed phenolic components such as lignan secoisolariciresinol diglucoside (SDG) and its metabolites along with p coumaric acid and ferulic acid glucosides were reported within in vitro models.  Moreover, the free radical scavenging activity of flaxseed phenolic components of n butanol fraction such as herbacetin 3, 8-0-diglucopynanoside, herbacetin 3, 7-0-diglucopyranoside, and (–) – pinoresinol diglucoside were also reported. In a previous study, the authors selectively isolated ether insoluble phenolic components such as tannins, caffeic acid, and phenolic glycosides from the n-butanol fraction of flaxseed, free from ether soluble phenolic components such as flavonoids, lignans etc. and reported their antioxidant potential in the in vitro models.  This study was undertaken to evaluate the role of these ether insoluble phenolic components of n-butanol fraction (EPC BF) of flaxseed in alleviation of hepatotoxicity resulting from carbon tetrachloride (CCI) intoxication through biochemical and histological parameters. In the present study hepatoprotective potential of EPC BF was assessed against carbon tetrachloride (CCI) intoxication in rats.  Hepatoxin CCI is converted to trichloromethyl (CCI) and then peroxy-radicals (CCI 00) by chytochrome P450 enzymes in liver.  These free radicals and reactive oxygen species (ROS) then initiate lipid peroxidation and resulted into damage of liver. Here, increased activities of enzymes AST, ALT, ALP, and total bilirubin levels were observed in CCI control group, which could be due to the CCI intoxicated increased oxidative stress.  The pretreatment of EPC BF to rats at doses 250 and 500 mg/kg, p.o. resulted into restoration of increased activities AST, ALT, ALP, and total bilirubin at the normal level, which could be mediated through neutralizing free radicals induced by CCI toxicity. In CCI intoxicated group, TBARS level is increased due to tissue damage and failure of antioxidant defense mechanism.  The animals treated with EPC BF shows reduced levels of CCI induced lipid peroxidation, which could be mediated through antioxidant defenses of EPC BF. Rats treated with EPC BF showed almost normal hepatic cellular architecture similar to control and silymarin treated rat groups.  This confirmed the hepatic structural integrity maintenance property of EPC BF, as shown by the hepatoprotective drugs. In conclusion, Reesults of current investigation first time demonstrated that EPC BF has significant hepatoprotective potential, which is likely related to its antioxidant potential.  Furthermore, this study also suggested that EPC BF could be largely contributed in hepatoprotective activity observed by flaxseed supplementation and it may have potential clinical application in therapy for liver diseases. (Editors comments)



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