| Biotechnology |
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| Hypothetical mode of action of earthworm extract with hepatoprotective and antioxidant properties |
| Mariappan BALAMURUGAN, Kasi PARTHASARATHI, Lalpet Souri RANGANATHAN, Edwin L. COOPER |
| Division of Vermibiotechnology, Department of Zoology, Annamalai University, Annamalai Nagar-608002, India; VLB Janakiammal College of Arts and Science, Kovaipudur, Coimbatore-641042, India; Laboratory of Comparative Immunology, Department of Neurobiology, UCLA Medical Centre, University of California Los Angeles, California 90095-1763, USA |
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Abstract The hepatoprotective potential of earthworm extract (EE) (Lampito mauritii, Kinberg) was evaluated against paracetamol-induced liver injury in Wistar albino rat, in comparison with silymarin, the standard hepatoprotective drug. We observed a reduction in liver antioxidants, such as glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) and in serum total protein, and an increase in serum alkaline phosphatase (ALP), serum aspertate aminotranferase (AST), serum alanine aminotranferase (ALT), bilirubin and liver thiobarbituric acid reactive substances (TBARS) due to liver injury in the paracetamol-administered rats (2 g/kg). On the contrary, increased activities of liver GSH, SOD, GPx, CAT and serum total protein level, and decrease in the contents of serum ALP, AST, ALT, bilirubin and liver TBARS were observed in rats administered with different doses of EE (100, 200 and 300 mg/kg), which are similar to the activities of hepatoprotective drug silymarin (150 mg/kg). The mode of action of EE as evidenced by the above parameters may suggest that EE, on the one hand, prevents the formation of the reactive oxygen groups, or scavenges these groups, thereby preventing the damage on the hepatic cells, and, on the other hand, modulates the genes responsible for synthesis of antioxidant enzymes such as GPx, CAT and SOD in liver tissue and decreases the serum enzymatic activities such as ALP, AST and ALT.
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Received: 27 August 2007
Published: 16 January 2008
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