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

AIM

To observe the effect of hypoxia/reoxygenation on the adherence of neutrophils to cardiomyocytes and to investigate the effect of ICAM-1/LFA-1 on hypoxia/reoxygenation injury of cardiomyocytes mediated by neutrophils.

METHODS

Count adhered neutrophils to cardiomyocytes suffering hypoxia, hypoxia/reoxygenation 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 with normal culture group (P < 0.01). The neutrophils to cardiomyocytes with hypoxia/reoxygenation were significantly increased compared lease 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/reoxygenation 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 neutrophils to hypoxia/reoxygenation cardiomyocytes. Anti-ICAM-1 and anti-LFA-1 antibody attenuated the cytotoxic effects of neutrophils on hypoxia/reoxygenated 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.