[Effect of ischemic preconditioning on human lung cell apoptosis in vivo and the expression of regulating gene bcl-2].

OBJECTIVE: To investigate whether ischemic reperfusion injury induces lung cell apoptosis and the effect of ischemic preconditioning on lung cell apoptosis by altering the expression of bcl-2 protein. METHODS: Sixteen patients, who needed to occlude the main pulmonary artery to undergo pulmonectomy, were randomly put to two groups: the control group (Group C) and the ischemic preconditioning group (Group I). Ischemic preconditioning was achieved by two 5-minute cycles of ischemic, and each was followed by a 5-minute reperfusion. The lung tissue was sampled at the time of preoccluding, 30 minutes after the ischemic, and 30 and 60 minutes after the reperfusion. Apoptotic cells were stained by the terminal deoxynucleotidyl transferase-mediated dUTP nickend labeling (TUNEL) technique. Immunohistochemistry was used to detect the expression of bcl-2 protein. RESULTS: The apoptosis index (AI) of lung cells increased significantly 30 and 60 minutes after the reperfusion, and also significantly increased as the reperfusion period prolonged. Apoptosis was significantly reduced in Group I 30 and 60 minutes after the reperfusion compared with that of Group C at the same time points (P < 0.05). Immunohistochemistry analysis showed that the expression of bcl-2 protein significantly increased in Group I compared with that of Group C(P < 0.05), while there was no significant difference at each time point in Group C(P > 0.05). CONCLUSION: 1. Ischemic reperfusion injury may induce human lung cell apoptosis. 2. Ischemic preconditioning may reduce the apoptosis of human lung cells in vivo by upregulating bcl-2 protein expression.