从内质网应激探讨针刺对脑缺血再灌注损伤保护作用机制

凋亡是公认的脑缺血病理过程的重要一环，而针刺通过调节凋亡基因表达，发挥其脑保护的作用，但机制尚未明确。脑缺血可引发内质网应激（ERS），GRP78和CHOP分别开启ERS时神经元的生存途径和凋亡途径。过强或持续时间过长的ERS通过PERK-eIF2α-ATF4-CHOP启动细胞凋亡。因此PERK通路及GRP78和CHOP表达对脑缺血有至关重要的作用。而针刺在这方面的实验研究未见报道。因此，本研究拟建立大鼠脑缺血再灌注模型，以针刺内关、百会穴为干预手段，以大鼠行为学和脑组织形态学为效应指标，通过观察造模和针刺前后GRP78和CHOP表达，分析针刺对脑缺血诱发ERS的影响。同时观察PERK-eIF2α-ATF4-CHOP凋亡通路因子变化，探讨针刺抗凋亡保护脑组织的内在机制之一是否与内质网应激PERK通路机制有关。同时以依达拉奉为对比，观察上述指标的变化，为临床选择有效的干预方法提供实验依据。

Apoptosis is an important part of the cerebral ischemia and the pathological process recognized acupuncture by regulating the expression of apoptotic genes play the role of cerebral protection, but the mechanism is not yet clear. Cerebral ischemia can lead to endoplasmic reticulum stress (ERS), GRP78 and CHOP, respectively, on the ERS neuron survival pathways and apoptotic pathways. The ERS is too strong or duration is too long to initiate apoptosis through the PERK-eIF2α-ATF4-with CHOP. PERK pathway, GRP78 and CHOP expression has a crucial role against cerebral ischemia. Experimental study of acupuncture in this area have not been reported. Therefore, this study before and after the establishment of cerebral ischemia and reperfusion model off to acupuncture Baihui interventions, rats behavior and cerebral morphology effect indicators, by observing the model and acupuncture GRP78 and CHOP expression, analysis of the impact of acupuncture on cerebral ischemia induced ERS. One of the internal mechanism of anti-apoptotic protection of brain tissue at the same time observe the PERK-eIF2α-ATF4-CHOP apoptosis pathway factor, and to explore acupuncture and endoplasmic reticulum stress the PERK pathway mechanism. At the same time provide experimental basis for effective intervention method for clinical edaravone regarded as a contrast, to observe the changes in these indicators.