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目的探讨小牛血清去蛋白注射液(DCSI)对脑缺血再灌注后大鼠海马Caspase-12表达的影响。方法健康SD大鼠随机分为假手术组、模型组和DCSI组。DCSI组于术前1 w开始给药,每日大鼠尾静脉注射DCSI 80 mg/kg,末次给药5 h后建立脑缺血再灌注模型。分别在脑缺血再灌注后的5个时间点进行神经行为学观察,海马病理学、细胞凋亡、Caspase-12蛋白及mRNA表达指标的检测。结果与假手术组相比,模型组大鼠脑缺血再灌注后的神经功能缺损明显,海马细胞呈明显凋亡表现,Caspase-12蛋白及mRNA表达上调,尤以24 h时明显(P<0.01);DCSI组与模型组相比,功能缺损评分和细胞凋亡相对较轻,Caspase-12蛋白及mRNA表达也相对下调(P<0.01,P<0.05)。结论 DCSI对缺血再灌注损伤大鼠大脑具有保护作用,其机制可能与其有效抑制脑组织Caspase-12 mRNA转录水平及蛋白表达、阻断内质网应激启动的凋亡通路有关。
Objective To investigate the effect of DCSI on Caspase-12 expression in rat hippocampus after cerebral ischemia-reperfusion. Methods Healthy SD rats were randomly divided into sham operation group, model group and DCSI group. The DCSI group was administrated 1 w preoperatively. DCSI 80 mg / kg was injected into the caudal vein of rats daily, and the cerebral ischemia-reperfusion model was established 5 h after the last administration. Neurobehavioral observation, hippocampal pathology, apoptosis, Caspase-12 protein and mRNA expression were detected at 5 time points after cerebral ischemia-reperfusion. Results Compared with the sham-operation group, the neurological deficits in the model group were obvious after cerebral ischemia and reperfusion, the apoptosis of hippocampal cells was obvious, the expression of Caspase-12 protein and mRNA were up-regulated, especially at 24 h (P < 0.01). Compared with the model group, the functional impairment score and apoptosis of DCSI group were relatively lighter, and the expression of Caspase-12 protein and mRNA were also down-regulated (P <0.01, P <0.05). Conclusion DCSI may have a protective effect on the brain of rats with ischemia-reperfusion injury. The mechanism may be related to the inhibition of the transcriptional level of Caspase-12 mRNA and the expression of protein, and the block of endoplasmic reticulum-triggered apoptosis pathway.