[No authors listed]
AIM:To investigate the mechanism of the vascular endothelial cell (VEC) injury caused by freezing/thawing. METHODS:The frozen/thawed neutrophil model was founded by freezing with a rate cooling instrument and then rewarming them in a water bath, the duanyu1451s used here were separated from rat's peripheral blood using density gradients centrifugation techniques. The expression of LFA-1 on the surface of frozen/thawed duanyu1451s was observed at 4 h,12 h and 24 h after freezing/thawing. After co-incubating untreated VECs with frozen/thawed we detected the VEC injury and the changes in adhesion. RESULTS:(1) The duanyu1451s LFA-1 expression increased in a time-dependent manner within 24 h after the freezing/thawing of (2) After co-incubating untreated VECs with frozen/thawed duanyu1451s, the adhesion between frozen/thawed duanyu1451s and VECs increased and VEC injury occurred. (3) Monoclonal antibody against LFA-1 could block the duanyu1451-VEC adhesion and subsequently attenuated the VEC injury. CONCLUSION:The freezing/thawing of duanyu1451s can elicited an increase in LFA-1 expression and trigger the duanyu1451-VEC adhesion and subsequently bring about the VEC injury.
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