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目的丁苯酞抗缺血性脑损害的细胞作用靶点。方法培养大鼠原代脑微血管内皮细胞(BMECs)及神经元,将2种细胞联合培养或将BMECs培养液预处理神经元后,予神经元氧糖剥夺损伤(OGD),计算神经元存活率,观察丁苯酞对其影响。结果丁苯酞不能直接提高神经元OGD损伤后的存活率,但能提高其中缺氧预处理及联合培养组的神经元OGD损伤后的存活率(P<0.05)。结论丁苯酞对神经元的保护作用依赖于BMECs的正常功能,提示其脑保护的直接细胞靶点是BMECs。
OBJECTIVE: To investigate the effect of Butylphthalide on the cell targets of ischemic brain damage. Methods Primary cultured rat brain microvascular endothelial cells (BMECs) and neurons were cultured in vitro. Two kinds of cells were co-cultured or pretreated with BMECs medium for neuronal oxygen glucose deprivation (OGD). Neuronal survival rates , Observe the impact of butylphthalide. Results Butylphthalide could not directly increase the survival rate of neurons after OGD injury, but could increase the survival rate of neurons in OGD group after hypoxic preconditioning and co-culture (P <0.05). Conclusion Butylphthalide has neuroprotective effects on the normal function of BMECs, suggesting that BMECs are directly targeted by brain protection.