丰富环境对大鼠脑缺血再灌注损伤后缺血半暗带区凋亡蛋白的影响

Effects of enriched environment on apoptosis protein in ischemic penumbra after cerebral ischemia reperfusion injury in rats

目的探讨丰富环境对大鼠脑缺血再灌注损伤后缺血半暗带区抗凋亡作用。方法建立大鼠局灶性脑缺血再灌注损伤模型,造模成功后分为假手术组(n=20)、标准环境模型组(n=20)、丰富环境模型组(n=20),分别在缺血再灌注1.5h后,在不同饲养环境中再分别饲养1、28d后,采用改良神经功能缺失(mNSS)评分对大鼠进行评估、苏木素-伊红(HE)染色观察缺血半暗带区细胞病理变化,免疫荧光、实时荧光定量聚合酶链反应(qPCR)检测缺血半暗带区域P53蛋白表达。结果 28d时,与标准环境模型组mNSS评分(9.83±1.17)分、免疫荧光P53蛋白表达(157.42±0.37)、实时荧光定量P53mRNA(2.36±0.12)比,丰富环境模型组mNSS评分(8.00±1.10)降低明显(P<0.05)、免疫荧光P53蛋白表达(129.43±0.42)明显减少,实时荧光定量P53mRNA(2.11±0.04)表达明显降低(P<0.01)。结论丰富环境处理对脑缺血再灌注损伤后大鼠有保护作用,作用机制可能是通过下调P53蛋白表达,从而抑制细胞凋亡的发生。

Objective To explore the anti-apoptosis effects of enriched environment on ischemic penumbra after cerebral ischemia reperfusion in rats.Methods Models of focal cerebral ischemia-reperfusion injury were established.After successful modeling,they were randomly divided into the sham group(n=20),the standard-environmental model group(n=20),and the rich-environment model group(n=20).After ischemia and reperfusion for 1.5 hours,they were breeded for 1 day and 28 days in different rearing environments respectively,rats were assessed using a modified neurological deficit score(mNSS),and HE staining was performed to observe cytopathologic changes in ischemic penumbra region.Immunofluorescence and real-time fluorescence quantitative(q-PCR)were used to detect P53 protein expression in ischemic penumbra.Results At the 28 th day,compared with the standard-environmental model group[mNSS score(9.83±1.17),expression of immunofluorescence P53 protein expression(157.42±0.37),real-time fluorescence quantitative P53 mRNA(2.36±0.12)],mNSS score(8.00±1.10),the expression of immunofluorescence P53 protein(129.43±0.42),and the real-time fluorescence quantitative P53 mRNA(2.11±0.04)were all significantly decreased in the enriched-environmental model group(P<0.01).Conclusion Enriched environmental treatment has protective effects on rats with cerebral ischemia-reperfusion injury,probably by down-regulating the expression of P53 protein and inhibiting the occurrence of cell apoptosis.