大鼠局灶性脑缺血损伤中表皮生长因子的表达变化的意义

Change of expression of epidermar growth factor in focal cerebral ischemia injury in rats

目的:探讨大鼠局灶性脑缺血损伤中脑组织内表皮生长因子受体(epidermargrowthfactorreceptor,EGFR)的表达变化及其意义。方法:选用雄性Wistar大鼠71只,采用自体血凝块注入颈内动脉的方法制作局灶性脑缺血2,4,6,12,24,48h模型,应用免疫组化及Western蛋白印迹分析方法检测脑组织中EGFR表达规律、时间依赖性及差异程度。结果:免疫组化结果EGFR在正常大脑皮质神经元中弱表达,EGFR在神经元中分布比较广泛,在神经元的胞膜、胞质及轴突均有表达。正常对照组与假手术组EGFR表达差异无显著性意义,在局灶性脑缺血损伤中随着缺血时间的延长,EGFR蛋白的表达逐渐增强,在缺血12h达高峰(147.11±7.36,182.71±8.23),尤以缺血半暗带区EGFR蛋白表达明显增强(182.71±8.23)。Western蛋白印迹分析结果,在局灶性脑缺血损伤中随着缺血时间的延长,缺血中心区及缺血半暗带区EGFR蛋白的表达逐渐增强,在缺血12h达高峰(20.087,26.174),尤以缺血半暗带区EGFR蛋白表达明显增强(26.174)。结论:局灶性脑缺血损伤可诱导神经元EGFR表达增加,EGFR表达增加可能与缺血神经元自身保护作用有关。

AIM:To explore the change and significance of expression of epidermar growth factor(EGFR) in the focal cerebral ischemia injury in rats. METHODS:Seventy one male Wistar rats were selected and made into focal ischemia models of 2, 4, 6, 12, 24, 48 h by injecting blood coagulum into internal carotid artery. Expressive regulation, time dependence and discrepancy degree of EGFR were tested in focal injury tissue with the methods of immunohistochemistry and western blotting trace analysis. RESULTS:The immunohistochemistry results showed that EGFR was low expression in normal cerebral cortex neurons. The distribution of EGFR in neurons was very extensive, and could be found in plasmalemma, neuroplasm and axis cylinder. There were no significant differences in the expression of EGFR between the pseudo operation group and the control group, expression of EGFR protein increased gradually with the time of ischemia, and reached the peak(147.11±7.36,182.71±8.23)at the 12th hour after ischemia. In the peri ischemia region EGFR increased significantly(182.71±8.23). The results of western blotting trace analysis showed that expression of EGFR protein increased gradually with the time of ischemia and reached the peak(20.087,26.174)at the 12th hour after ischemia in the center and peri ischemia region, and in the peri ischemia region EGFR increased significantly(26.174). CONCLUSION:The increase of neuron EGFR expression can be induced by focal cerebral ischemia injury, and may be related to the self protection of ischemia neurons.