Baicalin attenuates oxygen-glucose deprivationinduced injury by inhibiting oxidative stress-mediated 5-lipoxygenase activation in PC12 cells
Abstract
Aim: To determine whether the flavonoid baicalin attenuates oxygen-glucose deprivation (OGD)-induced injury by inhibiting oxidative stress-mediated 5-lipoxygenase (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 envelope 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.
Keywords:
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 envelope 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.