电针对脑缺血再灌注的Bax基因敲除小鼠的JNK线粒体通路的调控作用研究思路

Research design of regulation of electroacupuncture on the mitochondrial JNK signal pathway in cerebral ischemia-reperfusion mice with Bax gene knockout

目的探讨电针对脑缺血再灌注(I/R)的Bax基因敲除小鼠的JNK线粒体通路的调控作用研究思路。方法参考相关文献,结合前期研究发现,以研究假说的方式对电针对脑I/R的Bax基因敲除小鼠的JNK线粒体通路的调控作用进行论证阐述。结果脑I/R损伤可诱发神经细胞凋亡,在这个信号转导过程涉及多个基因的表达及相互作用,JNK信号通路介导的细胞凋亡在脑I/R损伤中起重要作用,肿瘤坏死因子α(TNF-α)、白细胞介素8(IL-8)是脑I/R形成的标志物,电针治疗可抑制神经细胞凋亡,减轻脑I/R损伤,保护神经元,应用Bax基因敲除小鼠使研究得以深化。结论研究以Bax基因敲除小鼠为基础,从JNK信号转导线粒体通路的不同环节—I/R模型、I/R特征、JNK活化、Bcl-2与Bax平衡、凋亡诱导因子(AIF)释放、细胞凋亡结果的多个层次,可以阐明电针调控脑I/R损伤海马神经元细胞凋亡的JNK信号转导caspase非依赖的线粒体通路机制。

Objective To study the research design of regulation of electroacupuncture on the mitochondrial JNK signal pathway in cerebral ischemia - reperfusion （I/R） mice with Bax gene knockout. Methods The research design was proved and explained by mean of research hypothesis with referenee literature combined with previous research results. Results Nerve cells apoptosis can be induced by cerebral I/R injury. This signal transduction processes involve more than one gene expression and the interaction. The cell apoptosis mediated by JNK signal pathway play an important role in cerebral I/R injury. The tumor necrosis taetor α（ TNF - α） and interleukin 8 （ IL - 8 ） was the marker for cerebral I/R. Electroacupuncture can inhibit the apoptosis of nerve cells,, reduce cerebral I/R injury, protect neurons. The application of Bax gene knockout made deepened the study. Conclusion This study illustrate the mechanism of the regulation and controlling of eleetroacupuneture on the JNK signal transduction caspase -independent mitochondrial pathways in cerebral I/R hippocampus neuron apoptosis which based on the Bax gene knockout mice, and explained from different aspects level covers the I/R model, I/R feature, JNK activation, thebalance of Bcl -2 and Bax, AIF release and cell apoptosis.