Baicalein Induction of Hydroxyl Radical Formation via 12-Lipoxygenase in Human Platelets: An ESR Study

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• 作者：Duen-Suey Chou ; Jie-Jen Lee ; George Hsiao ; Cheng-Ying Hsieh ; Yan-Jyu Tsai ; Tzeng-Fu Chen ; Joen-Rong Sheu
• 刊名：Journal of Agricultural and Food Chemistry
• 出版年：2007
• 出版时间：February 7, 2007
• 年：2007
• 卷：55
• 期：3
• 页码：649 - 655
• 全文大小：136K
• 年卷期：v.55,no.3(February 7, 2007)
• ISSN：1520-5118

文摘

The pro-oxidant activities of baicalein, morin, myricetin, quercetin, and rutin were examined in variouscell-containing systems including human platelets, rat vascular smooth muscle cells, human umbilicalvein endothelial cells (HUVECs), human THP-1 cells, and fibroblast cells. Electron spin resonance(ESR) results showed that only baicalein generated hydroxyl radicals in a resting human plateletsuspension, whereas the other flavonoids showed no effects on any of the resting cell systems. Alow concentration of arachidonic acid (AA) increased the intensity of hydroxyl radicals, but a highconcentration inhibited it. Collagen and thrombin, platelet aggregatory agents that can cause therelease of AA by platelets, enhanced baicalein-induced hydroxyl radical formation, whereas ADPand U44619 showed no significant effects. Quinacrine and 5,8,11,14-eicosatetraenoic trifluoromethylketone, both PLA₂ inhibitors, significantly attenuated baicalein-induced hydroxyl radical formation.These results suggest that baicalein-induced hydroxyl radical formation is associated with AAmetabolite enzymes in human platelets. The formation of hydroxyl radicals was significantly inhibitedby lipoxygenase inhibitors including nordihydroguaiaretic acid, (-)-epicatechin, (-)-epicatechin gallate,and hinokitiol, but was not affected by desferroxamine or the heme protein inhibitors KCN and NaN₃.On the other hand, semiquinone free radicals were generated when baicalein was incubated withhorseradish peroxidase/H₂O₂ or platelets/AA. The semiquinone radicals formed in the platelets/AAsystem could be extensively inhibited by desferroxamine, diethylenetriaminepentaacetic acid, KCN,and NaN₃, indicating that prostaglandin H synthase (PGHS)-peroxidase may be involved. The resultsof this study led to the proposal that baicalein induces hydroxyl radical formation via 12-lipoxygenaseand induces semiquinone radical formation via PGHS-peroxidase in human platelets.