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目的:对黄芩苷、胆酸、珍珠母及栀子苷在治疗脑缺血疾病中的药理通路变化及药理作用机制。方法:采取随机法将脑缺血模型小鼠分为黄芩苷组(BA组)、珍珠母组(CM组)、胆酸组(CA组)及栀子苷组(JA组)和模型组(M组),每组脑缺血模型小鼠20只。在其脑缺血2小时后,对其给于相应的药物进行治疗。24小时之后,对小鼠断头缺脑,提取其脑海马组织的总RNA。采用与小鼠脑缺血相关基因的芯片对其基因表达谱变化水平进行检测。利用数据处理软件对数据进行标准化处理之后,利用Arrytrack软件作为平台,选择黄芩苷组与模型组,栀子苷组与模型组,胆酸组与模型组及珍珠母组与模型组之间的差异基因,差异有统计学意义。按照Genebank,将几组之间的差异表达基因上传到Genego数据库。选择信号通路,根据每组P值,选择P值最小的前2位,对不同组分的药效机制进行分析。结果:黄芩苷组、珍珠母组、胆酸组及栀子苷组与模型组比较,其差异基因数量分别为45、31、55及51条。通过对四组分差异相似度最大的前2位信号通路能够得出结论,栀子苷组、胆酸组及珍珠母组在实验中,都参与存活于死亡,及信号通路(TNFR_1)的调控。同时,黄芩苷组则表现出对A2A及G蛋白信号具有调控功能。胆酸组主要表现为对NMDA具有依赖性的LTP调节作用。结论:黄芩苷主导抗调亡,胆酸作用为抗神经元变异及抑制钙离子内流方面,栀子苷在缺血后脑保护及抑制脑细胞凋亡方面效果显著,但是珍珠母效果则不太明显,其药理通路有待进一步研究。
OBJECTIVE: To study the pharmacological mechanism of baicalin, bile acid, nacre and geniposide in the treatment of cerebral ischemia. Methods: The cerebral ischemia model mice were randomly divided into four groups: BA group, CM group, CA group, JA group and model group M group), 20 mice in each group. After 2 hours of its cerebral ischemia, it was given the corresponding medicine for treatment. Twenty-four hours later, the mice were decapitated and their total RNA was extracted from the hippocampus. The level of gene expression profile was detected by using the chip with mouse cerebral ischemia-related genes. After using the data processing software to standardize the data, using Arrytrack software as a platform, the differences between the baicalin group and the model group, the geniposide group and the model group, the cholate group and the model group, and the mother of pearl group and the model group were selected Genes, the difference was statistically significant. According to Genebank, differential expression genes from several groups were uploaded into the Genego database. Select the signal path, according to each P value, select the P value of the first two, the pharmacodynamics of different components were analyzed. Results: Compared with model group, the number of differentially expressed genes in baicalin, nacre, cholic acid and geniposide groups were 45, 31, 55 and 51, respectively. Through the first two signal pathways with the highest similarity among the four components, it can be concluded that geniposide, bile acid and pearl mothers all participated in the death and the regulation of signal pathway (TNFR_1) . At the same time, baicalin group showed the regulation of A2A and G protein signals. Cholic acid group mainly manifested as dependent on the NMDA LTP regulatory role. CONCLUSION: Baicalin plays a key role in anti-apoptosis, anti-neuron mutation and inhibition of calcium influx. Geniposide has a significant effect on cerebral protection and inhibition of brain cell apoptosis after ischemia, but the effect of nacre Obviously, its pharmacological pathway needs further study.