| Inflammatory mechanism has been studied during ischemic cerebrovascular diseases in recent years. Researchers had observed that inflammatory cells, especially polymorphonuclear cells (PMNs) in first two days, infiltrated into focal cerebral tissue after cerebral ischemia/reperfusion injury in rats. PMNs infiltration would damage the cerebral tissue in different ways: (1) PMNs adhesion and infiltration could block the microvessels, decrease blood flow, and lead to "no reflow" phenomenon; (2)PMNs could produce abundant free radicals, induce lipid peroxidation. (3) PMNs could release many kinds of inflammatory mediator, such as leukotriene and prostaglandins, etc, to make microvessels contracting; (4) activated PMNs could release elastinase which could break down extracellular matrix to lead cerebral edema. But the mechanism of PMNs infiltration is unclear, nuclear factor kappa B(NF-кB), intercellular adhesion molecular-1 (1CAM-1) and macrophage inflammatory protein-1 (MIP-1), maybe play important roles in the process. The project studied the time course of these factors, and observed the expression of myeloperoxidase (MPO) reflecting PMNs infiltration by establishing rat cerebral ischemia/reperfusion (I/R) injury model. The object was aimed to study the roles of these factors during PMNs infiltration and to provide some theory for clinical treatment. Material and method:84 health, male SD rats, 260g -290g, were divided into control group(n =12), sham-operated group(n=12) and operated group (I/R Ih group, I/R 3h group, I/R 6h group, I/R 12h group, I/R 24h group, 12 per group). Rat transient cerebral ischemic injury model was established with suture emboli method. In operated group, rats were sacrificed at responding time point after Ihour of middle cerebral artery occlusion (MCAO). Sham-operated group were operated but nylon suture were just put into external carotid artery. In each group, 6 rats' brain made up into homogenate, were used to examine sICAM-1 and MIP-1 with ELISA method; 6 rats' brain embeded in paraffin, were used to examine NF-кB and myeloperoxidase (MPO) with immunohistochemistrical method. Then computer image analysis system was used to analyze the gray values of NF-кB and MPO. Results:1. There was no stained NF-кB-immunoreactive cells in control group and sham-operated group. Activated NF-кB-immunoreactive cell were observed at Ih after reperfusion(gray value was 99.95±4.82), peaked at 3 hours (gray value was 92.06 ± 3.38, P <0.05 compared to other time points), then decreased, but keeped in high level at 24 hours(gray value was 141.12 + 3.91). Neurons, astrocytes and microvascular endothecium were stained.2. Expression of sICAM-1 was low in control group and sham-operated group, raised at Ihour after reperfusion(62.09 ± 2.52ng/ml, P<0.05 compared to control group and sham-operated group), peaked at 12 hours( 160.21 ±3.05 ng/ml, P<0.05 compared to the other time points ), then decreased, but keeped in high level at 24 hours(133.91 ±3.05 ng/ml).3. Expression of MIP-1 was low in control group and sham-operated group, raised at Ihour after reperfusion(19.98 ± 2.13pg/ml, P<0.05 compared to control group and sham-operated group), peaked at 12 hours(61.34 ± 3.06 pg/ml, P<0.05 compared to the other time points ), then decreased, but keeped in high level at 24 hours(49.46 ± 3.08 pg/ml).4. There was no stained MPO-immunoreactive cells in the control group, sham-operated group, 1 hour and 3 hours after reperfusion. Activated MPO-immunoreactive cell were observed at 6h after reperfusion (gray value was 150.88 + 4.68), peaked at 24 hours (gray value was 82.22 ±3.96, P <0.05 compared to the other time points). Conclusion:1. The research evidenced that PMNs infiltration played an important role in the cerebral ischemia /reperfusion injury in rat.2. NF-кB took part in the cerebral ischemia/reperfusion injury in rat, the mechanism maybe due to promote expression of ICAM-1 and MIP-1, then to aggravate PMNs infiltration.3. ICAM-1 and MIP-1 to...
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