Abstract: The mechanisms by which breviscapine (Bre) inhibits the lipid preoxidation in rat brain mitochondria were investigated. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by thiobarbituric acid spectrophotometry. The chelating activities of Bre for Fe²⁺ were tested by differential spectrum. Superoxide anion (O2^·-) from xanthine-xanthine oxidase (Xan-XO) system and hydroxyl radical (·OH) from FeSO4-H2O2 system were determined with spectrophotometry. It was found that Bre could effectively inhibit the lipid peroxidation of brain mitochondria induced by free radicals driven from Xan-XO and FeSO4-H2O2 system. The IC50 of Bre were 93.01 μmol·L-1 for Xan-XO system and 62.18 μmol·L^-1 for FeSO4-H2O2 system. Bre also scavenged O2^·- and ·OH produced by Xan-XO and FeSO4-H2O2 systems. The IC50 of Bre were 32.63 μmol·L^-1 for O2^·- and 20.22 μmol·L^-1 for ·OH. Furthermore, the chelating Fe²⁺ activity of Bre was shown. It may be concluded that Bre inhibited lipid peroxidation at different stages of the reaction of oxygen free redial with the mitochondria membrane: (1) the formation of ·OH; (2) the initiation of the lipid peroxidation, by chelating Fe²⁺ and scavenging O2^·- as well as ·OH. The scavenging oxygen free radicals and chelating iron are the mechanisms of inhibitory effect of Bre on lipid peroxidation.

Key words: Breviscapine, Brain mitochondria, Lipid peroxidation, Oxygen free radical, Chelator