QUENCHING OF N-NITROSOPYRROLIDINE INDUCED HEPATOCELLULAR CARCINOMA ON POST TREATMENT WITH THE HELICTERES ISORA

摘要

Objective: The present study was aimed at probing the protective potential of Helicteres isora hydroethanolic stem bark extract (HIHSBE) against N-nitrosopyrrolidine (NPYR) induced hepatocellular carcinoma (HCC) in Swiss albino male mice. Method: Mice were divided into six groups of six mice in each. Hepatocellular carcinoma (HCC) was induced by single intraperitoneal injection of the carcinogen nitrosopyrrolidine (NPYR). Followed by the subcutaneous injection of carbon tetrachloride (CCl4). Carcinogen treated mice were then orally administered with Helicteres isora hydroethanolic stem bark extract (HIHSBE) at a dose of 100 and 200 mg/kg once daily for 4 weeks followed by investigation of liver injury markers like alanine transaminase (ALT), aspartate transaminase (AST), alanine phosphatase (ALP), gamma glutamyl transferase (GGT), Lactate dehydrogenase (LDH). Tumor markers alpha fetoprotein and carcinoembryonic antigen were determined in serum. Level of catalase (CAT), reduced glutathione (GSH), glutathione-s- transferase (GST) and lipid peroxidation were also estimated. Results: The level of liver injury markers and antioxidant enzymes decreased in the liver tissue of NPYR treated mice compared to normal control mice. However, HIHSBE post treatment increased the level of these enzymes compared to only carcinogen treated mice. HIHSBE also lowered the level of tumor markers and lipid peroxidation in serum and liver tissue of mice bearing HCC respectively. Histological studies also supported biochemical investigations. Conclusion: The chemopreventive effect of HIHSBE is well supported in our study as it hinders the development of HCC by interacting with ROS during carcinogenesis and thus counterbalancing the antioxidant defense system as analyzed.