Liu Lu-Ying, Wei Er-Qing, Zhao Yan-Min, Chen Fang-Xue, Wang Meng-Ling, Zhang Wei-Ping, Chen Zhong
Department of Pharmacology, School of Medicine, Zhejiang University, 353, Yan An Road, Hangzhou 310031, P. R. of China.
J Pharm Pharmacol. 2005 Aug;57(8):1019-26. doi: 10.1211/0022357056622.
Baicalin is a flavonoid derivative from Scutellaria baicalensis Georgi with various pharmacological effects. Recently, the neuroprotective effect of baicalin was reported. To confirm this effect and explore the possible mechanism, we have investigated the protective effect of baicalin on ischaemiclike or excitotoxic injury and the activation of protein kinase C alpha (PKC(alpha)) in rat hippocampal slices. In-vitro ischaemic-like injury was induced by oxygen/glucose deprivation (OGD) and the excitotoxic injury by N-methyl-D-aspartate (NMDA). The viability and swelling of the slices were detected by triphenyltetrazolium chloride (TTC) staining and image analysis of light transmittance (LT), respectively. The translocation of PKC(alpha) was measured by immunoblotting. Baicalin was added during both injuries. Baicalin (0.1, 1, and 10 micromol L(-1)) concentration-dependently inhibited OGD-induced viability reduction and acute neuron swelling, and inhibited the increased portion of PKC(alpha) present in the membrane fraction over the total PKC(alpha). Baicalin ameliorated NMDA-induced viability reduction (not LT elevation) and inhibited the NMDA-increased membrane portion of PKC(alpha) at 1 micromol L(-1). We concluded that baicalin had a protective effect on ischaemic-like or excitotoxic injury in rat hippocampal slices, which might have been partly related to inhibition of PKC(alpha) translocation.
黄芩苷是一种从黄芩中提取的黄酮类衍生物,具有多种药理作用。最近,有报道称黄芩苷具有神经保护作用。为了证实这一作用并探究其可能的机制,我们研究了黄芩苷对大鼠海马切片缺血样或兴奋毒性损伤的保护作用以及蛋白激酶Cα(PKCα)的激活情况。体外缺血样损伤通过氧糖剥夺(OGD)诱导,兴奋毒性损伤通过N-甲基-D-天冬氨酸(NMDA)诱导。分别通过氯化三苯基四氮唑(TTC)染色和透光率(LT)图像分析检测切片的活力和肿胀情况。通过免疫印迹法测定PKCα的转位。在两种损伤过程中均加入黄芩苷。黄芩苷(0.1、1和10 μmol L-1)浓度依赖性地抑制OGD诱导的活力降低和急性神经元肿胀,并抑制膜组分中PKCα相对于总PKCα增加的部分。黄芩苷改善了NMDA诱导的活力降低(而非LT升高),并在1 μmol L-1时抑制了NMDA增加的PKCα膜组分。我们得出结论,黄芩苷对大鼠海马切片的缺血样或兴奋毒性损伤具有保护作用,这可能部分与抑制PKCα转位有关。