正常新生大鼠及缺血缺氧性损伤后脑组织铁的组织化学改变
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Histochemical Expression of Iron in the Brain of Normal and Hypoxic Ischemic Insulted Neonatal Rats
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    摘要:

    目的:应用大鼠HIE模型了解正常情况下及缺血缺氧损伤后脑组织铁的组织化学改变。方法:实验分正常对照组和HIE组。正常对照组分别于 8 d,10 d,14 d,21 d 龄处死(每时间点3只),HIE组分别于 7 d 龄大鼠(HIE)模型制成后观察 12 h,24 h,3 d,7 d,14 d 处死(每时间点3只)。各组脑组织切片,进行铁Perl's染色和光镜观察。结果:正常大鼠脑组织铁染色阳性细胞较少且主要见于扣带及胼胝体、脑室周围、内囊及外囊的尖部。形态学上铁染色阳性细胞主要与少突神经胶质细胞和小神经胶质细胞相似。HIE组缺血缺氧损伤后 12 h 脑组织铁染色情况与正常对照组无明显差异。缺血缺氧损伤后随时间推移铁染色逐渐增强,1周时为甚,以皮质、内囊及海马回处最明显,铁染色阳性神经胶质的增多程度大于铁染色阳性细胞的增多程度,有明显的傍血管现象。结论:铁染色可作为判断脑组织缺血缺氧中晚期损伤程度的指标之一。

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    OBJECTIVE: To study the iron histochemical expression in the brain of normal and hypoxic ischemic insulted neonatal rats. METHODS: The iron histochemical changes in the brain were observed under the light microscope at 12 h, 24 h, 3 d, 7 d and 14 d after the hypoxic ischemic encephalopathy (HIE) model was established (HIE group, n=15). Brain sections were stained by the perl's method. Twelve normal age matched neonatal rats were used as the controls. RESULTS: In the controls, there were small patches of iron positive cells located mainly in the corpus callosum and cingulum, periventricular zone, internal capsule, and tip of the external capsule. Morphologically, iron positive cells resembled oligodendrocytes and microglia. There was no significant difference in the positive staining between the HIE group and controls at 12 h after HI. At 24 h after HI, the number of iron positive cells started to increase in the ipsilateral hemisphere in the HIE group. There was apparently positive staining of glia and paravascular positive staining foci. The positive staining further increased time dependently and peaked at 7 d after HI in the cortex, internal capsule and hippocapus. At 14 d after HI, the number of iron positive cells decreased yet did not return to normal. CONCLUSIONS: Brain iron histochemistry is upregulated after HI insult and it could be used to assess the degree of cerebral damage in the moderate or late stage.

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黑明燕, 旷寿金, 殷萍.正常新生大鼠及缺血缺氧性损伤后脑组织铁的组织化学改变[J].中国当代儿科杂志,2002,4(6):445-447

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