Effects of human thioredoxin on pneumocyte apoptosis and Bcl-2/Bax expression in rats with lung ischemia/reperfusion injury

AIM: To explore the relationship between apoptosis in the lung tissues and lung ischemia/reperfusion injury, and to observe the effects of human thioredoxin (hTrx) on apoptosis in lung ischemia/reperfusion injury. METHODS: The single lung in situ ischemia/reperfusion animal model was used. Eighty four Wistar rats were randomly divided into control group (control), groups of ischemia for 1 h and reperfusion for different times (IR1h, IR3h, IR5h), and groups of IR+human thioredoxin treatment (IR1h +hTrx, IR3h +hTrx and IR5h +hTrx). Transmission electron microscope (TEM), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and immunocytochemistry techniques were used to observe apoptosis, apoptosis signal-regulating kinase 1 (ASK1) and expression of Bcl-2 and Bax in various phases of lung ischemia/reperfusion. RESULTS: Cell apoptosis in lung tissues was significantly high, ASK1, Bcl-2 and Bax protein were up-regulated in lung tissues of lung ischemia/reperfusion injury as compared to control (all P<0.01). Compared to IR group, hTrx suppressed apoptosis as well as expression of ASK1 and Bax protein (P<0.01), Bcl-2 protein and the ratio of Bcl-2/Bax were up-regulated in lung tissues (all P<0.05 or P<0.01). There was a significant correlation between the expression of ASK1, Bax protein and cell apoptosis (r=0.775, r=0.814, respectively; all P<0.01). There was a negative correlation between cell apoptosis and Bcl-2/Bax protein (r=-0.275, P<0.05). CONCLUSION: Initiating cell apoptosis by the activation of Bcl-2/Bax system in lung tissues may contribute to the pathogenesis of lung ischemia/reperfusion injury. The protective effects of hTrx include suppressing the expression of ASK1, down-regulating the ratio of Bcl-2/Bax and blocking apoptosis in lung tissues in lung ischemia/ reperfusion injury.