论文部分内容阅读
目的:探讨原花青素(procyanidin,PC)对脑缺血再灌注后大鼠海马内质网应激(endoplasmic re-ticulum stress,ERS)相关分子表达的影响。方法:将180只SD大鼠随机分为假手术组、模型组和PC组,每组60只。PC组于术前1周灌胃给予PC(100 mg.kg-1)然后建立脑缺血再灌注模型,分别在脑缺血再灌注后3,6,12,24和48 h处死大鼠。观察不同时间点大鼠的神经行为表现;焦油紫染色处理大鼠海马组织切片,光镜观察病理学改变;末端标记法(TUNEL)检测细胞凋亡;采用免疫组化及RT-PCR方法检测脑缺血再灌注后不同时间点大鼠海马GRP78和CHOP的表达。结果:PC组大鼠脑缺血再灌注后的神经功能缺损明显改善,与模型组相比具有统计学差异(P<0.01),其细胞凋亡数亦明显少于模型组(P<0.05);模型组与假手术组相比,GRP78与CHOP明显升高(P<0.01),PC组GRP78表达高于模型组(P<0.05),而PC组CHOP表达低于模型组(P<0.05)。结论:PC对脑缺血再灌注损伤大鼠具有保护作用,其机制可能与其增加GRP78表达、拮抗CHOP表达、阻断内质网应激(ERS)启动的凋亡通路有关。
Objective: To investigate the effect of procyanidin (PC) on the expression of ERS in rats hippocampus after cerebral ischemia / reperfusion. Methods: 180 SD rats were randomly divided into sham operation group, model group and PC group, 60 rats in each group. The PC group was given intragastric administration of PC (100 mg.kg-1) one week before operation, then the model of cerebral ischemia / reperfusion was established. Rats were sacrificed at 3, 6, 12, 24 and 48 h after cerebral ischemia-reperfusion. The neurobehavioral performance of rats at different time points was observed. The hippocampal tissue sections of rats were treated with tar violet staining, the pathological changes were observed by light microscope, the apoptosis was detected by TUNEL, the brain was detected by immunohistochemistry and RT-PCR The expression of GRP78 and CHOP in hippocampus of rats at different time points after ischemia reperfusion. Results: Compared with the model group, the neurological deficit in PC group was significantly improved (P <0.01) and the number of apoptotic cells in model group was significantly lower than that in model group (P <0.05) (P <0.01). The expression of GRP78 in PC group was higher than that in model group (P <0.05), while the expression of CHOP in PC group was lower than that in model group (P <0.05) . CONCLUSION: PC may have a protective effect on cerebral ischemia-reperfusion injury in rats. The mechanism may be related to increasing the expression of GRP78, antagonizing the expression of CHOP and blocking the apoptotic pathway initiated by endoplasmic reticulum stress (ERS).