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ARTICLE

Butein imparts free radical scavenging, anti-oxidative and proapoptotic properties in the flower extracts of Butea monosperma

ANURADHA SEHRAWAT AND VIJAY KUMAR^*

Virology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi 110067, India.

*Address correspondence to: Vijay Kumar. E-mail:

BIOCELL 2012, 36(2), 63-71. https://doi.org/10.32604/biocell.2012.36.063

Abstract

The flower of Butea monosperma (Lam.) (Fabaceae) has been used in traditional Indian medicine in the treatment of many ailments including liver disorders. To understand the pharmacological basis of its beneficial effects, the extracts of dried flowers in water, methanol, butanol, ethyl acetate and acetone were evaluated for free radical scavenging and pro-apoptotic activities in cell cultures (human hepatoma Huh-7 cell line and immortalized AML-12 mouse hepatocytes). Butrin and butein -the active constituents of flower extracts- were used as reference molecules. The levels of cell injury markers like lactate dehydrogenase, glutathione and lipid peroxidation and primary antioxidant enzymes glutathione S-transferase and catalase were also measured. The aqueous and butanolic extracts exhibited better 2,2-diphenyl-1-picrylhydrazyl scavenging and cytotoxic activities in hepatoma cells than in immortalized hepatocytes. Interestingly, butein inhibited 2,2-diphenyl-1-picrylhydrazyl radical better than butrin. The aqueous and butanolic extracts were further investigated for hepatoprotection against carbon tertrachloride-induced biochemical changes and cell death. Both extracts, just as butrin and butein, significantly reversed the cellular glutathione levels and lipid peroxidation, and glutathione–S-transferase activity. Lactate dehydrogenase leakage and cell death were also prevented. However, only butein revived the catalase activity. Thus, the butein content of Butea monosperma flower extracts is important for free radical scavenging activity, apoptotic cell death and protection against oxidative injury in hepatic cells.

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