大鼠局灶脑缺血诱导巢蛋白的反应模式

目的:观察巢蛋白(nestin)在局灶脑缺血区的反应模式,以探讨其在脑梗塞灶修复过程中的作用。方法:采用局灶脑缺血模型和免疫组织化学染色方法,探查36只成年雄性SD大鼠的大脑不同区域的巢蛋白阳性细胞的形态、反应时程和分布形式。结果:假手术大鼠的巢蛋白阳性反应存在小血管、微血管和室管膜上皮,在第三脑室底壁内有许多细的阳性纤维,胞体不明显。在脑缺血3 d组,大量巢蛋白阳性细胞分布于缺血侧大脑半球,以大脑皮质缺血区、视前区、尾壳核及第三脑室底部最为显著。缺血区周围的大脑皮质浅层和视前区皮质的阳性细胞呈纤维状,而皮质深层的阳性细胞则呈星状。 巢蛋白阳性细胞的形态和数量变化在脑缺血1周时最显著。阳性细胞显示高度的肥大和增生性变化,其数量亦明显增加,以大脑皮质缺血区和尾壳核区最显著。皮质缺血区和尾壳核区的巢蛋白阳性反应持续到脑缺血6周。随后,其反应稍有减弱。结论:局灶脑缺血诱导反应型星形胶质细胞重表达巢蛋白,提示其可能参与脑缺血性损伤的修复过程。

A reactive pattern of ischemia-induced nestin protein in the rat brain

AIM: To explore the expressive profile of nestin protein in the focal ischemic brain and to study the recovery mechanism of brain focal infarct . METHODS: Cellular morphology, time-course and distribution pattern of nestin positive response were immunohistochemically examined in different brain regions of 36 adult male SD rats. RESULTS: Nestin positive response of different brain regions in sham operated rats was present in small- and micro-vasculartures and the third ventricle bottom and ependyma. A large number of nestin positive cells were detected in ischemic brain, and were more remarkable in the cortical areas of parietal lobe and preoptic area as well as ischemic caudoputamen. Stellate nestin positive cells were located in the deep layer of ischemic cortex, but fibrillary cells were located in the shallow layer. Nestin positive cells in the ischemic caudoputamen showed the same changes of morphology as those cells in the deep layer of ischemic cortex. Morphological and number alterations of nestin positive cells were the most remarkable at 1 weeks post-ischemia, which showed more hypertrophy and proliferation in morphology, and a marked increase in number was present in the ischemic cerebral cortex and the ischemic caudoputamen. These alterations of nestin positive cells persisted up to 6 weeks post-ischemia, and then, the nestin positive response in the ischemic brain decreased gradually. CONCLUSION: Focal cerebral ischemia induces nestin re-expression on reactive astrocytes, which may be very important to the self-recovery of cerebral infarct.