Department of Pharmacology, Zhejiang University, Hangzhou, China.
Acta Pharmacol Sin. 2010 Feb;31(2):137-44. doi: 10.1038/aps.2009.196.
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.
The effects of baicalin and the 5-LOX inhibitor zileuton on the changes induced by OGD/recovery or H(2)O(2) (an exogenous reactive oxygen species [ROS]) in green fluorescent protein-5-LOX-transfected PC12 cells were compared.
Both baicalin and zileuton attenuated OGD/recovery- and H(2)O(2)-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 H(2)O(2). In contrast, zileuton did not show these effects.
Baicalin can inhibit 5-LOX activation after ischemic injury, which may partly result from inhibition of the ROS/p38 mitogen-activated protein kinase pathway.
探讨黄芩苷是否通过抑制氧化应激介导的 5-脂氧合酶（5-LOX）激活来减轻 PC12 细胞氧葡萄糖剥夺（OGD）诱导的损伤。
比较黄芩苷和 5-LOX 抑制剂齐留通对 OGD/复氧或 H₂O₂（外源性活性氧 [ROS]）诱导转染绿色荧光蛋白-5-LOX 的 PC12 细胞变化的影响。
黄芩苷和齐留通均能浓度依赖性地减轻 OGD/复氧和 H₂O₂诱导的损伤，并抑制 OGD/复氧诱导的 5-LOX 代谢产物（半胱氨酰白三烯）的产生。然而，黄芩苷并未降低基础半胱氨酰白三烯水平。黄芩苷还可减少 OGD/复氧诱导的 ROS 产生，并抑制 OGD/复氧和 H₂O₂诱导的 5-LOX 向核膜易位和 p38 磷酸化。相比之下，齐留通则没有显示出这些效果。
黄芩苷可抑制缺血性损伤后 5-LOX 的激活，这可能部分是由于抑制了 ROS/p38 丝裂原活化蛋白激酶途径。
