Molecular and Cellular Biochemistry

, Volume 238, Issue 1, pp 181–186

Schisandrin B protects against tert-butylhydroperoxide induced cerebral toxicity by enhancing glutathione antioxidant status in mouse brain

  • Kam-Ming Ko
  • Brian Y.H. Lam

DOI: 10.1023/A:1019907316129

Cite this article as:
Ko, KM. & Lam, B.Y. Mol Cell Biochem (2002) 238: 181. doi:10.1023/A:1019907316129


Schisandrin B (Sch B), a dibenzocyclooctadiene derivative isolated from Fructus Schisandrae, has been shown to produce antioxidant effect on rodent liver and heart. A mouse model of tert-butylhydroperoxide (t-BHP) induced cerebral toxicity was adopted for examining the antioxidant potential of Sch B in the brain. Intracerebroventricular injection of t-BHP caused a time-dependent increase in mortality rate in mice. The t-BHP toxicity was associated with an increase in the extent of cerebral lipid peroxidation and an impairment in cerebral glutathione antioxidant status, as evidenced by the abrupt decrease in reduced glutathione (GSH) level and the inhibition of Se-glutathione peroxidase activity at 5 min following t-BHP challenge. Sch B pretreatment (1 or 2 mmol/kg/day × 3) produced a dose-dependent protection against t-BHP induced mortality. The protection was associated with a decrease in the extent of lipid peroxidation and an enhancement in glutathione antioxidant status in brain tissue detectable at 5 min post t-BHP challenge, with the assessed biochemical parameters being returned to normal values at 60 min in Sch B pretreated mice at a dose of 2 mmol/kg. The ensemble of results suggests the antioxidant potential of Sch B pretreatment in protecting against cerebral oxidative stress.

Schisandra chinensis schisandrin B glutathione glutathione peroxidase oxidative brain injury 

Copyright information

© Kluwer Academic Publishers 2002

Authors and Affiliations

  • Kam-Ming Ko
    • 1
  • Brian Y.H. Lam
    • 1
  1. 1.Department of BiochemistryThe Hong Kong University of Science and TechnologyClear Water BayHong Kong, China

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