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目的探讨外源性降钙素基因相关肽(CGRP)和神经生长因子(NGF)对短暂性全脑缺血后再灌注大鼠纹皮质c-junmRNA及蛋白表达的影响。方法原位杂交和免疫组织化学结合显微图像分析方法。结果假手术组大鼠纹皮质c-junmRNA表达弱;缺血组较假手术组c-junmRNA表达显著强(P<0.01);CGRP组和NGF组c-junmRNA表达弱于缺血组(P<0.05);CGRP和NGF合用组c-junmRNA表达明显弱于缺血组(P<0.01),分别弱于CGRP组和NGF组(P<0.05)。假手术组大鼠纹皮质未见c-Jun蛋白表达;缺血组较假手术组c-Jun蛋白表达明显强(P<0.01),缺血后再灌注3 h强,1 d、3 d时弱;CGRP组和NGF组c-Jun蛋白表达较缺血组弱(P<0.05);CGRP和NGF合用组较缺血组c-Jun蛋白表达明显弱(P<0.01),分别弱于CGRP组和NGF组(P<0.05);CGRP和NGF合用组缺血后再灌注3 h时强,1 d、3 d时弱。结论CGRP和NGF分别抑制全脑缺血后再灌注大鼠纹皮质c-junmRNA及蛋白表达,联合应用显著抑制全脑缺血后再灌注大鼠纹皮质c-junmRNA及蛋白表达,两者对保护缺血神经元可能有协同作用。
Objective To investigate the effects of exogenous calcitonin gene related peptide (CGRP) and nerve growth factor (NGF) on c-jun mRNA and protein expression in rat striatum after transient global cerebral ischemia. Methods In situ hybridization and immunohistochemistry combined with microscopic image analysis. Results The expression of c-jun mRNA in the striatum of rats in sham-operation group was weak. The expression of c-jun mRNA in ischemic group was significantly higher than that in sham operation group (P <0.01). The expression of c-jun mRNA in CGRP group and NGF group was weaker than that in ischemia group 0.05). The expression of c-jun mRNA in CGRP group and NGF group was weaker than that in ischemia group (P <0.01), but lower than that in CGRP group and NGF group (P <0.05). The c-Jun protein expression was not observed in the striate cortex of rats in sham operation group. The expression of c-Jun protein in ischemic group was significantly higher than that in sham operated group (P <0.01) The expression of c-Jun in CGRP group and NGF group was weaker than that in ischemia group (P <0.05). The expression of c-Jun protein in CGRP group and NGF group was weaker than that in ischemia group (P <0.01) And NGF group (P <0.05). The combination of CGRP and NGF group was stronger at 3 h after reperfusion and weaker at 1 d and 3 d. Conclusions CGRP and NGF can inhibit c-jun mRNA and protein expression of striate cortex in rats after global cerebral ischemia and reperfusion, respectively. Combination therapy can significantly inhibit c-jun mRNA and protein expression in striate cortex of rats after global cerebral ischemia. Ischemic neurons may have synergistic effects.