Baicalin attenuates oxygen-glucose deprivation- induced injury by inhibiting oxidative stress-mediated 5-lipoxygenase activation in PC12 cells

Aim： To determine whether the flavonoid baicalin attenuates oxygen-glucose deprivation （OGD）-induced injury by inhibiting oxidative stress-mediated 5-1ipoxygenase （5-LOX） activation in PC12 cells. Methods： The effects of baicalin and the 5-LOX inhibitor zileuton on the changes induced by OGD/recover...

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Published in:Acta pharmacologica Sinica 2010-02, Vol.31 (2), p.137-144
Main Authors: Li, Cheng-tan, Zhang, Wei-ping, Fang, San-hua, Lu, Yun-bi, Zhang, Li-hui, Qi, Ling-ling, Huang, Xue-qin, Huang, Xiao-jia, Wei, Er-qing
Format: Article
Language:English
Subjects:
Animals
Arachidonate 5-Lipoxygenase - metabolism
Enzyme Activation
Flavonoids - pharmacology
Glucose - metabolism
Hydrogen Peroxide - metabolism
Original
Oxidative Stress
Oxygen - metabolism
p38 Mitogen-Activated Protein Kinases - metabolism
PC12 Cells
PC12细胞
Phosphorylation
Rats
Reactive Oxygen Species - metabolism
氧化应激
细胞损伤
葡萄糖
酶激活
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Summary:Aim： To determine whether the flavonoid baicalin attenuates oxygen-glucose deprivation （OGD）-induced injury by inhibiting oxidative stress-mediated 5-1ipoxygenase （5-LOX） activation in PC12 cells. Methods： The effects of baicalin and the 5-LOX inhibitor zileuton on the changes induced by OGD/recovery or H2O2 （an exogenous reactive oxygen species [ROS]） in green fluorescent protein-5-LOX-transfected PC12 cells were compared. Results： Both baicalin and zileuton attenuated OGD/recovery- and H2O2-induced injury and inhibited OGD/recovery-induced production of 5-LOX metabolites （cysteinyl leukotrienes） in a concentration-dependent manner. However, baicalin did not reduce baseline cysteinyl leukotriene levels. Baicalin also reduced OGD/recovery-induced ROS production and inhibited 5-LOX translocation to the nuclear enve- lope and p38 phosphorylation induced by OGD/recovery and H2O2. In contrast, zileuton did not show these effects. Conclusion： Baicalin can inhibit 5-LOX activation after ischemic injury, which may partly result from inhibition of the ROS/p38 mitogenactivated protein kinase pathway.
ISSN:1671-4083
1745-7254
DOI:10.1038/aps.2009.196