Liv.52 protects HepG2 cells from oxidative damage induced by tert-butyl hydroperoxide

• Published in: Molecular and cellular biochemistry 2010, Vol.333 (1-2), p.41-48
• Main Authors: Vidyashankar, S, Mitra, S.K, Nandakumar, Krishna S
• Format: Article
• Language: English
• Subjects: Antioxidants; Antioxidants - pharmacology; Biochemistry; Biomedical and Life Sciences; Cardiology; Cell Death; Cellular biology; Complications and side effects; Cytotoxicity; Drug Combinations; Enzymes; Glutathione; Hep G2 Cells; Herbal medicine; Humans; Iron compounds; Life Sciences; Lipid Peroxidation; Liver; Liver - metabolism; Liver - pathology; Medical Biochemistry; Oncology; Oxidative stress; Oxidative Stress - drug effects; Peroxidation; Plant Extracts - pharmacology; Plant Extracts - therapeutic use; Telomerase; tert-Butylhydroperoxide - toxicity; Toxicants
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-009-0202-6

Oxidative stress induced by toxicants is known to cause various complications in the liver. Herbal drug such as Liv.52 is found to have hepatoprotective effect. However, the biochemical mechanism involved in the Liv.52 mediated protection against toxicity is not well elucidated using suitable in vitro models. Hence, in the present study, the hepatoprotective effect of Liv.52 against oxidative damage induced by tert-butyl hydroperoxide (t-BHP) in HepG2 cells was evaluated in order to relate in vitro antioxidant activity with cytoprotective effects. Cytotoxicity was measured by MTT assay. Antioxidant effect of Liv.52 was determined by 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay, ferric-reducing antioxidant power (FRAP) assay, and lipid peroxidation and measurement of non-enzymic and antioxidant enzymes in HepG2 cells exposed to t-BHP over a period of 24 h. The results obtained indicate that t-BHP induced cell damage in HepG2 cells as shown by significant increase in lipid peroxidation as well as decreased levels of reduced glutathione (GSH). Liv.52 significantly decreased toxicity induced by t-BHP in HepG2 cells. Liv.52 was also significantly decreased lipid peroxidation and prevented GSH depletion in HepG2 cells induced by t-BHP. Therefore, Liv.52 appeared to be important for cell survival when exposed to t-BHP. The protective effect of Liv.52 against cell death evoked by t-BHP was probably achieved by preventing intracellular GSH depletion and lipid peroxidation. The results showed protective effect of Liv.52 against oxidative damage induced in HepG2 cells. Hence, taken together, these findings derived from the present study suggest the beneficial effect of Liv.52 in regulating oxidative stress induced in liver by toxicants.