| Background and Purpose:In recent 20 years, we have made great development in the study of the pathological mechahisms of the ischaemic cerebrovascular disease. The research on inflammatory response of cerebral ischemia and cytokines has become a central issue.The inflammatory response is caused the expression of preinflammatory cytokines .Tumor necrosis factor is the preinflammatory cytokine on which a good study has been made. One of its injury functions to cerebralis is excessive inflammatory response. Through induced molecule protein change of leukocytes and endothelial cell, the release of TNF-a promotes the adhesion of the to endothelial cell. The infiltrated leukocytes expresses GD11/CD18 adhesion molecule, while endothelial cell expresses intercellular adhesion molecule-1, (1CAM).1-CAM-1 plays an important role in cerebral ischemia and reperfusioninjury. It can be used as fragment antigen binding of function antigen of leukocytes, which contributes to the adhesion of the leukocytes to blood vessel endothelium, movement and effusion of the leukocytes. At the same time, it joins in inflammatory response.Soluble intercellular adhesion molecule exists in people's serum. It covers the most part of external arch of adhesion molecule on the surface of cell mantians its binding function. At present, little is known about the release order and net relationship of adhesion molecule and cell factor in the course of cerebral ischema injury. This study was made , through examination and measurement of TNF-a, s1CAM-1 in the serum of acute cerebral infarction, and observation of their changes and relation, to investigate the change of serum tumornecrosisfactor-α(TNF-α) and solubal intercellular adhesion molecul e-1(sICAM-1) with acute cerebral infarction and its clinical significance and delve into their functional mechanisms which may cause cerebral ischema injury. And it will provide theoretical basis for the clinical unti-inflammatory treatment of (cerebral anaemia) and their interference of different inflammatory sectors.Materials and Methods: The level of serum TNF-α and sICAM-1 was measured serially with two-layer antibody sandwich enzyme linked immunosorbent assay(ELISA) in 53 patients with acute cerebral infarction in 1 day, 3day 7day and 14 day after onset, 32 patients with cerebalatherosclerosis(CAS) and 36 normal controls. Then the relationship between them was analyzed and compared.Statistic analysis: material expression applies average ±standard deviation(X±S). Experimental data adopts SPSS version 10.0 statistic software analysis. First respective comparison between average numbers of many samples has employed varian homoscedasticity testing and one-way analysis of variance. Then the comparison has been made respectively with LSD. The correlation between group variable has adopted linear correlation analysis.Results: It was shown that: (1) the level of serum TNF-α and sICAM-1 in patients with cerebral infarction increased from 1 days after onset to 3 days and decreased from after 3 days to 7 days ,and almost to the level of nomal controls in 14 days; the level of serum TNF-α and sICAM-1 in patients with cerebral infarction 1 days, 3 days, 7 days after the onset was significantly higher than that in patients with CAS and normal controls (P<0.01); the level of serum TNF-α and sICAM-1 was not difference in patients with CAS and normal controls as well cerebral infarction 14 days after the onset. (2) the level of serum TNF-a and the level of sICAM-1 were positively correlated in patients with cerebral infarction in 1 days,3 days , 7 days after onset( P<0.05). (3) the level of serum TNF-α and sICAM-1 in patients with cerebral infarction 3 days after onset was significantly difference in the patients with large and medium as well small cerebral infarction (P<0.01); the level of serum TNF-α and the level of sICAM-1were significantly correlated in patients 3 days after onset with large and medium and small cerebral infarction(P<0.01),and the correlation was fund 1 da... |
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