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作 者:晋凌云[1] 刘嘉瀛[1] 杨增仁[1] 颜培华[1]
机构地区:[1]军事医学科学院卫生学环境医学研究所,天津300050
出 处:《中国应用生理学杂志》2005年第4期393-396,共4页Chinese Journal of Applied Physiology
摘 要:目的:探讨肿瘤坏死因子-α(TNF-α)在组织冻融造成的血管内皮细胞(VEC)损伤过程中的作用。方法:以右旋糖酐沉降法分离的大鼠嗜中性粒细胞(PMN)和体外培养的大鼠VEC为实验材料,建立细胞冻融模型。通过测定培养液中LDH活性确定VEC损伤程度,采用活性染料吞噬法检测与VEC粘附的PMN数,以流式细胞技术分析淋巴细胞功能相关抗原-1(LFA-1)表达。结果:TNF-α上调冻融PMN表面LFA-1表达,促进冻融PMN与正常VEC粘附,增强VEC损伤。抗LFA-1Mab部分阻断冻融PMN与正常VEC粘附,减轻VEC损伤。结论:在冻融损伤过程中TNF-α促进PMN表面LFA-1表达,增强PMN-VEC粘附,加重VEC损伤。Aim:To investigate the role of TNF-α in vascular endothelial cells injury mediated by freezing/thaw ing PMN. Methods: Freezing/thawing cell model was founded using rat PMN isolated by dextran sedimentation technique and VEC cultured in vitro. The injury level of VEC was indicated by measuring activity of LDH in medium. The number of frozen/thawed PMN adhering to VEC was counted with Phagocytizing reactive dyes the degree of frozen/thawed PMN and VEC adhesion, Expression of LFA-1 on the surface of frozen/thawed PMN was analyzed with flow cytometry. Results: TNF-α could obviously upregulate expression of LFA-1 on surfaced of frozen/thawed PMN. Upregulation of LFA-1 expression promoted adhesion of frozen/thawed PMN and normal VEC,and aggravated VEC injury. Monoclonal antibody against LFA-1 could partly block adhesion of frozen/thawed PMN and normal VEC,and attenuate VEC injury. Conclusion : TNF-α can promote expression of LFA- 1 on surface of frozen/thawed PMN adhering of frozen/thawed PMN to normal VEC and VEC injury increase, monoclonal antibody against LFA-1 could partly block PMN-VEC adhesion and attenuate VEC injury.
关 键 词:冻融损伤 嗜中性粒细胞 血管内皮细胞 肿瘤坏死因子-α 淋巴细胞功能相关抗原-1
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