International Journal of Medicine and Medical Sciences Vol. 3(8), pp. 252-255, August 2011 Available online http://www.academicjournals.org/ijmms ISSN 2006-9723 ©2011 Academic Journals Full Length Research Paper Hepatoprotective potentials of Butea monosperma stem bark extract against carbon tetrachloride induced hepatotoxicity in albino rats Prashant Tiwari 1 *, Kuldeep Kumar 2 , Rajnikant Panik 3 , Alok Pandey 4 , Ashish Pandey 4 and Pratap Kumar Sahu 4 1 Pinnacle Biomedical Research Institute Bhopal, Madhya Pradesh, India. 2 Smt. Vidyawati Collage of Pharmacy, Jhansi Uttar Pradesh, India. 3 Government Girls Polytechnic, Baron Bazar, Raipur, Chhattisgarh, India. 4 Raipur Institute of Technology, Raipur Chhattisgarh, India. 5 Siksha ‘O’ Anusandhan University, Bhubaneswar, Orissa, Bhubaneswar, India. Accepted 13 June, 2011 Carbon tetrachloride (CCl 4 ) pharmacological tool was used to produce liver damage in rats. Silymarin (100 mg/kg) and extract of Butea monosperma (shown to be hepatoprotective substances) prevented the CCl 4 induced toxicity. Hydroalcholic extract of the stem bark of B. monosperma was evaluated for its hepatoprotective. This in vitro efficacy was reinforced by a significant dose dependent hepatoprotection (at 100 and 200 mg/kg dose) by decreasing the activity of serum enzymes, bilirubin, and lipid peroxidation while it significantly increased the reduced Glutathione levels of tissue in a dose dependant manner. The hepatoprotective activities of the extract are being comparable to standards Silymarin. The results obtained in the present study indicate that stem bark extract of B. monosperma is a potential source of natural hepatoprotective. The hepatoprotective property may be attributed to the antioxidant potential and the phytochemical constituents of the plant. The present study justifies the claim of the native practitioner that the decoction of the plant is useful in treating jaundice and find out the clinical efficacy of the B. monosperma. Key words: Carbon tetrachloride, Butea monosperma, silymarin, alanine amino transferase, glutathione, serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, hepatoprotection. INTRODUCTION Hepatic system is a very vital organ system involved in the body’s metabolic activities. As a result the chemical reactions in the liver may generate several reactive *Corresponding author. E-mail: ptc_ptc15@rediffmail.com. Abbreviations: CCl4, Carbon tetrachloride; CCl3, trichloromethyl radical; CCl3O2, trichloromethylperoxy radical; SGOT, serum gluataic oxaloacetate transaminase; SGPT, serum glutamic pyruvic tranaminase; MDA, malonaldehyde; ALP, alkaline phosphate; GR, glutathione reductase; TCA, tissue glutathione; DTNB, 5, 5 Dithio-bis 2- nitrobenzoic acid; ANOVA, analysis of variance; TCA, trichloroacetate; TBA, tribromoanisole; HCl, hydrochloric acid; GPx, glutathione peroxidase; SOD, superoxide dismutase. species like free radicals. These reactive species form covalent bond with the lipids of the tissue. However inbuilt protective mechanisms combat the hazardous reactions associated with the free radicals. Due to exces- sive exposure to hazardous chemicals, the free radicals generated will be so high such that they overpower the natural defensive system leading to hepatic damage and cause jaundice, cirrhosis and fatty liver, which remain one of the serious health problems. Carbon tetrachloride (CCl 4 ) is one of such hazardous chemicals which induces hepatopathy through membrane lipid peroxidation by its free radical derivatives, trichloromethyl radical (CCl 3 •) and trichloromethylperoxy radical (CCl 3 O 2 •). Excessive pro- duction of the reactive species manifests in tissuethiol depletion, lipid peroxidation, plasma membrane damage etc., culminating into severe hepatic injury (Chrungoo et