细胞粘附分子在中性粒细胞介导的缺氧／复氧心肌细胞损伤中的作用

目的观察缺氧/复氧对心肌细胞与中性粒细胞粘附效应的影响及细胞间粘附分子-1(intercellularadhensionmolecule-1,ICAM-1)和淋巴细胞功能相关抗原-1(lymphocytefunctionassociatedantigen-1,LFA-1)在中性粒细胞介导的心肌细胞损伤的作用。方法计数不同实验条件下与心肌细胞粘附的中性粒细胞;以及抗ICAM-1单抗和抗LFA-1单抗阻断后中性粒细胞粘附数的改变,检测心肌细胞乳酸脱氢酶释放量。结果中性粒细胞与缺氧/复氧心肌细胞粘附数较缺氧组和正常对照组显著增加(P＜0.01);心肌细胞释放LDH明显增高(P＜0．01),单纯缺氧组与正常对照组相比无显著差异(P＞0．05)。加入抗ICAM-1单抗和抗LFA-1单抗后,缺氧/复氧组与心肌细胞粘附的中性粒细胞数较正常对照组显著降低(P<0．01),心肌细胞释放LDH也明显下降(P＜0．01)。缺氧组与正常对照组相比则无显著差异(P＞0.05)。结论缺氧/复氧使心肌细胞与中性粒细胞粘附效应增加,心肌细胞损伤加重,ICAM-1和LFA-1参与这一过程。抗ICAM-1和抗LFA-1单抗可减轻中性粒细胞对缺氧/复氧心肌细胞的损伤。

Effect of ICAM-1/LFA-1 on hypoxia/reoxygenation injury of cardiomyocytes mediated by neutrophils

Aim: To observe the effect of hypoxia/reoxgenation on the adherence of neutrophils to cardiomyocytes and to investigate the effect of ICAM 1/LFA 1 on hypoxia/reoxgenation injury of cardiomyocytes mediated by neutrophils. Methods: Count adhered neutrophils to cardiomycytes suffering hypoxia, hypoxia/reoxgenation and normal culture, as well as adhered neutrophils that were blocked by anti ICAM 1 and LFA 1 monoclonal antibodies. Release of lactate dehydrogenase (LDH) was determined as injury index of cardiomyocytes. Results: Adherence of neutrophils to cardiomyocytes with hypoxia/reoxgenation were significantly increased compared with normal culture group( P <0.01). The release of LDH by cardiomyocytes was also significantly increased( P <0.01). There was no significant difference between hypoxia group and normal control( P >0.05). The adherence of neutrophils to hypoxia/reoxgenation cardiomyocytes was significantly inhibited by anti ICAM 1 and anti LFA 1 antibody compared with normal culture group( P <0.01). While release of LDH markedly decreased( P <0.01). Conclusions: Hypoxia/reoxygenation increased the adherence of neutrophils to cardiomyocytes. ICAM 1 and LFA 1 mediated the enhanced adherence of neutrophits to hypoxia/reoxygenation cardiomyocytes. Anti ICAM 1 and anti LFA 1 antibody attenuated the cytotoxic effects of neutrophils on hypoxia/reoxygenate cardiomyocytes. These results suggested that the damage of neutrophils on cardiomyocytes is partly mediated by ICAM 1/LFA 1. Anti ICAM 1 and LFA 1 antibody are both beneficial in protecting hypoxia/reoxygenation cardiomyocytes from injury mediated by neutrophils.