Cerebral blood flow disturbances lead to the massive death of brain cells. The death of >80% of cells is observed in hippocampal cell cultures after 40 min of oxygen and glucose deprivation (ischemia-like conditions, OGD). However, there are some populations of GABAergic neurons which are characterized by increased vulnerability to oxygen-glucose deprivation conditions. Using fluorescent microscopy, immunocytochemical assay, vitality tests and PCR-analysis, we have shown that population of GABAergic neurons are characterized by a different (faster) Ca²⁺ dynamics in response to OGD and increased basal ROS production under OGD conditions. A plant flavonoid taxifolin inhibited an excessive ROS production and an irreversible cytosolic Ca²⁺ concentration increase in GABAergic neurons, preventing the death of these neurons and further excitation of a neuronal network; neuroprotective effect of taxifolin increased after incubation of 24 h and correlated with increased expression of antiapoptocic and antioxidant genes Stat3 Nrf-2 Bcl-2, Bcl-xL, Ikk2, and genes coding for AMPA and kainate receptor subunits; in addition, taxifolin decreased expression of prooxidant enzyme NOS and proinflammatory cytokine IL-1β.

脑血流障碍导致脑细胞大量死亡。在缺氧和缺糖40分钟后（缺血样情况，OGD），在海马细胞培养物中观察到> 80％的细胞死亡。但是，有些群体的GABA能神经元的特征是对氧-葡萄糖剥夺条件的脆弱性增加。使用荧光显微镜，免疫细胞化学测定，活力测试和PCR分析，我们已经表明，在OGD条件下，响应OGD的GABA能神经元群体具有不同的（较快的）Ca ²⁺动态，并且增加了基础ROS的产生。植物类黄酮类滑素抑制过量的ROS产生和不可逆的胞质Ca ²⁺GABA能神经元的浓度增加，防止这些神经元死亡并进一步刺激神经元网络；孵育24小时后，taxefolin的神经保护作用增强，并且与抗凋亡和抗氧化基因Stat3 Nrf-2 Bcl-2，Bcl-xL，Ikk2以及编码AMPA和红藻氨酸受体亚基的基因表达增加相关；另外，滑石粉降低了前氧化酶NOS和促炎细胞因子IL-1β的表达。