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根据sadrozaden报道的方法复制胎鼠海马神经细胞原代培养缺糖损伤模型 ,采用细胞形态学、DNA裂解率、流式细胞仪方法 ,观察缺糖损伤后 ,原代培养的胎鼠海马CA1神经细胞的形态结构 ,DNA完整性、神经细胞发生凋亡的数量 ;结果 ,缺糖损伤后 ,培养神经细胞DNA裂解率随时间延长而增加 ,12h达到 83 % ,脑溢安颗粒剂 (NYA)对缺糖损伤后神经细胞DNA裂解率的抑制作用大于模型组 ,差异具有统计学意义 (P <0 0 5 ) ;流式细胞仪器检测 ,在 12h时间点 ,NYA组神经细胞凋亡数量比模型组减少 37% ,差异具有统计学意义 (P <0 0 5 )。本研究提示 ,NYA具有抑制培养神经细胞DNA断裂 ,减少神经细胞凋亡的作用。
According to the method reported by Sadrozaden, primary rat models of hypoxic-ischemic injury of hippocampal neurons were replicated, and primary cultured rat hippocampal CA1 neurons were observed after anoxia-induced injury using cell morphology, DNA fragmentation, and flow cytometry. The morphological structure, DNA integrity, and the number of apoptotic cells in nerve cells; as a result, the DNA lysis rate of cultured neurons increases with the prolongation of time after a glucose deprivation injury, reaching 83% at 12h, and the Niaoyao granules (NYA) deficiency. The inhibitory effect of saccharin-damaged cells on the DNA lysis rate was greater than that of the model group (P < 0.05). The number of neuronal cell apoptosis in the NYA group was lower than that in the model group at 12h after flow cytometry. 37%, the difference was statistically significant (P < 0 05). This study suggests that NYA has the effect of inhibiting neuronal DNA breaks and reducing neuronal apoptosis.