Evaluation of Antioxidant and Hepatoprotective Effect of Acacia modesta Wall against Paracetamol Induced Hepatotoxicity

Aims: Aim of present study was to investigate the protective effect of Acacia modesta bark (Am. Cr) and its proposed mechanism against Paracetamol-induced hepatotoxicity in mice.
Study Design: Albino mice (20-30 g) of either sex were divided into five groups with six animals in each. Group-I was considered as–ve control (received normal saline), Group-II as + ve control (received paracetamol), while Group-III, IV and V as trail (received crud extract of A. modesta bark 12.5, 25 and 50 mg/kg respectively). Blood samples were collected by cardiac puncture for analysis of different markers of hepatotoxicity.
Place and Duration of Study: Faculty of Pharmacy, The University of Lahore, Lahore, Pakistan, between April 2013 and 0ctober 2013.
Methodology: Hepatotoxicity was assessed by evaluation of serum levels of hepatic metabolic enzymes; alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and metabolic content; Bilirubin and level of plasma proteins synthesize by liver (albumin and globulin), by using Randox Test Kits and biochemical analyzer Microlab 300 respectively. The antioxidant effect of Am.Cr was assayed through in vitro analysis of free radical scavenging activity by using DPPH (2, 2-diphenyl-1-picrylhydrazyl) solution.
Results: Am. Cr decreases the hepatic enzymes; AST, ALT and ALP, which indicates that Am.Cr contain hepatoprotective constituent(s). Am. Cr bark extract protected against decrease in serum Albumin and Total Protein levels caused by Paracetamol. Am. Cr also showed a good antioxidant activity comparable to Ascorbic acid. Presence of antioxidant constituent(s) was also supported by Tannins and saponins, found during phytochemical analyses of crude extract.
Conclusion: The results indicate the presence of hepatoprotective constituent(s) in extract of A. modesta bark and give the logical bases for the use of A. modesta as hepatoprotective regime and strongly suggest that this hepatoprotective effect is due to the presence of MDME (microsomal drug metabolizing enzyme) inhibition and antioxidant activity.