Cellular apoptosis and Bcl-XL/Bax expression in lung during total hepatic ischemia-reperfusion in rats

Objective To explore the relationship of cellular apoptosis and expression of Bcl-XL/Bax in lung during total hepatic ischemia/reperfusion (I/R) in rats , and its importance in lung injury. Methods 48 healthy male SD rats were randomly divided into 6 groups(n=8): ① pre-ischemia group, ② reperfusion 0 h group, ③ reperfusion 0.5 h group, ④ reperfusion 1h group, ⑤ reperfusion 3 h group, ⑥ reperfusion 6 h group.Total hepatic I/R was developed by occlusion of hepatic helium for 30 minutes, and the occlusion was then released for reperfusion. 48 healthy male Sprague Dawley rats weighing 250 g -300 g were killed respectively prior to ischemia and at 0, 0.5, 1, 3,6 h after reperfusion, and the lung tissue was taken for determination of apoptotic cells, Bel-XL mRNA, Bax mRNA expression, wet/dry(W/D) ratio and histological examination. Results After hepatic I/R the W / D ratio (4.96±0.25, 5.30±0.32, 5.36±0.32, 5.71±0.33, 5.32±0.28)and apoptotic index (4.86±0.64)%, (7.64±0.61)%, (15.60± 0.59)%, (19.74±0.71)%and (27.48±0.88)% were increased respectively (P<0.05), compared with preischemia (4.59±0.24)% and (4.00±0.45)%. Bcl-XL/Bax ratio after hepatic I/R (1.01±0.13, 0.43±0.03, 0.51±0.07, 0.62±0.06, 0.62±0.07) were decreased (P< 0.01), compared with preischemia (1.48±0.11). Histological examination revealed that the alveolar architecture was destroyed, with interstitial thickening and neutrophil infiltration after hepatic I/R. Correlation analysis indicated that the apoptotic index showed a positive correlation with the W/D ratio (r= 0.56, P<0.01 ) and a negative correlation with the Bcl-XL/Bax ratio (r=-0.55, P<0.01). Conclusion Total hepatic ischemia-reperfusion in rats could lead to aggravation of pneumocyte apoptosis, which promoted acute lung injury. Reduction of Bcl-XL/Bax ratio during this period might mediate the occurrence of apoptosis . Key words: Apoptosis ;  Bcl-XL ;  Bax ;  Reperfusion injury ;