【摘要】 目的探讨丹参酮对大鼠神经细胞脑缺血样损伤模型的保护作用及其机制。方法采用组织培养法，以原代大鼠大脑皮层神经细胞为材料，制备缺糖损伤、缺氧损伤、自由基损伤、咖啡因损伤、一氧化氮损伤及ＮＭＤＡ毒性损伤模型，细胞形态学观察神经细胞损伤变化，结晶紫活细胞染色后测定ＯＤ值。结果形态学检查发现丹参酮对６种脑缺血样损伤模型中的大鼠神经细胞具有明显保护作用，结晶紫染色也提示丹参酮可显著提高损伤模型中神经细胞的存活数，同等剂量条件下，丹参酮对自由基损伤、咖啡因损伤及ＮＭＤＡ毒性损伤的保护作用优于其余各组。结论丹参酮对上述６种大鼠神经细胞缺血损伤均有保护作用。更多还原

【Abstract】 AIM To investigate protective effects and mechanism of tanshinones on ischemia-like injury models. METHODS Six ischemia models including hypoxia, hypoglucose, oxidant injury, caffeine injury, nitric oxide neurotoxicity and excitatory amino acid injury were used to assay the anti-ischemic roles of tanshinones in cultured primary cortex neurons. The changes of injuried cortex neurons were observed by the way of morphological examination, and live neurons of crystal violet staining were measured according to absorbent index. RESULTS it was found that tanshinones possessed obvious protective effects on primary neurons in injury models by the way of morphological e~nation. Crystal violet staining also indicated that tanshinones increased number of live neurons in injury models significantly. The protective effects of tanshinones on models of oxidant injury, caffeine injury and NMDA injury were superior to other injury models. CONCLUSIONS 83.0 μmol· L- 1 tanshinones protected rat cortex cells fm all injury models effectively in vitro.更多还原