β-Glucuronidase inhibitor tectorigenin isolated from the flower of Pueraria thunbergiana protects carbon tetrachloride-induced liver injury
Article first published online: 30 JUL 2003
Volume 23, Issue 4, pages 221–226, August 2003
How to Cite
Lee, H.-W., Choo, M.-K., Bae, E.-A. and Kim, D.-H. (2003), β-Glucuronidase inhibitor tectorigenin isolated from the flower of Pueraria thunbergiana protects carbon tetrachloride-induced liver injury. Liver International, 23: 221–226. doi: 10.1034/j.1600-0676.2003.00830.x
- Issue published online: 30 JUL 2003
- Article first published online: 30 JUL 2003
- Received 13 January 2003, accepted 25 March 2003
- liver injury;
Background/Aim: To understand the relationship between the fluctuation in serum β-glucuronidase and hepatotoxicity, an inhibitor of β-glucuronidase was isolated from the flowers of Pueraria thunbergiana and its hepatoprotective activity was measured.
Method: Tectorigenin was isolated from the flowers of pueria thunbergiana as an inhibitor of β-glucuronidase, and serum ALT, AST and biological parameters as markers for its hepatoprotective activity were measured on CCl4-induced liver injury in mice. The relationship between serum β-glucuronidase and hepatoprotective activities in mice was measured.
Results: When tectorigenin at a dose of 100 mg/kg was intraperitoneally administered on CCl4-induced liver injury in mice, it significantly inhibited the increase of plasma ALT, AST and LDH activities. The inhibitory effect of tectorigenin is much more potent than that of dimethyl diphenyl bicarboxylate (DDB), which has been used as a commercial hepatoprotective agent. When tectoridin transformed to tectorigenin by intestinal bacteria was orally administered to mice, it showed hepatoprotective activity. However, when tectoridin was intraperitoneally administrated to mice, it did not exhibit hepatoprotective activity. Moreover, orally administered tectoridin not only inhibited β-glucuronidase but also increased GSH content and GST activity on CCl4-induced hepatotoxicity of mice.
Conclusion: We insist that an inhibitor of β-glucuronidase tectorigenin may be hepatoprotective and tectoridin should be a prodrug transformed to tectorigenin.