银杏内酯B对神经细胞活性影响的实验研究

目的 研究不同剂量银杏内酯B对低血清培养体系中神经细胞活性的影响。方法 将新生Wister大鼠大脑皮层神经细胞分别培养在含10％小牛血清(对照组)、5％小牛血清(低血清组)、5％小牛血清 0．1mg／L银杏内酯B(0．1mg／L银杏内酯组)、5％小牛血清 1mg／L银杏内酯B(1mg／L银杏内酯组)、5％小牛血清 10mg／L银杏内酯B(10mg／L银杏内酯组)、5％小牛血清 40mg／L银杏内酯B(40mg／L银杏内酯组)、5％小牛血清 100mg／L银杏内酯B(100mg／L银杏内酯组)的DMEM培养液中，通过MTT比色法，分别检测各组神经细胞的活性。结果 培养第2、5、8天与对照组比较，低血清组、0.1mg／L和1mg／L银杏内酯组神经细胞活性均明显下降；与低血清组比较，0．1mg／L和1mg／L银杏内酯组细胞活性均无明显改变；而10mg／L、40mg／L和100mg／L银杏内酯组细胞的活性均明显升高。结论 银杏内酯B在10～100mg／L浓度范围内，能增强5％小牛血清体系中的神经细胞活性。

The effects of ginkgolide B on the activity of neurons

Objective To investigate the effects of ginkgolide B on the activity of damaged neurons induced by calf serum deficiency in different concentrations.Methods Cortical neurons of newborn Wister rat were cultured in different conditions as follows:DMEM containing calf serum (10%) serving as control group;DMEM containing calf serum (5%) as the group of low calf serum;DMEM containing calf serum (5%) and ginkgolide B (0.1mg/L) serving as the group of 0.1mg/L of ginkgolide B;DMEM containing calf serum (5%) and ginkgolide B (1mg/L) serving as the group of 1mg/L of ginkgolide B;DMEM containing calf serum (5%) and ginkgolide B (10mg/L) serving as the group of 10mg/L of ginkgolide B;DMEM containing calf serum (5%) and ginkgolide B (40mg/L) serving as the group of 40mg/L of ginkgolide B;DMEM containing calf serum (5%) and ginkgolide B (100mg/L) serving as the group of 100mg/L of ginkgolide B.The activity of cultured neurons was measured by MTT colorimetric assay.Results At days of 2?5?8 respectively,compared with the control group,the activity of neurons of the groups of low calf serum,0.1mg/L of ginkgolide B and 1mg/L of ginkgolide B decreased significantly.Compared with the group of low calf serum,the activity of neurons of the groups of 0.1mg/L and 1mg/L of ginkgodide B was not enhanced significantly, but the activity of neurons of the groups of 10mg/L?40mg/L and 100mg/L of ginkgolide was enhanced significantly. Conclusion Ginkgolide B at the concentrations of 10~100mg/L could enhance the activity of damaged neurons induced by calf serum deficiency.