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."/>
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
Abstract：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.
HEI Ming-Yan,KUANG Shou-Jin,YIN Ping. Histochemical Expression of Iron in the Brain of Normal and Hypoxic Ischemic Insulted Neonatal Rats[J]. CJCP, 2002, 4(6): 445-447.
