Abstract: [Abstract] Objective To investigate the effect of intermittent hypoxia (IH) with pulmonary emphysema on the expression of hypoxia inducible factor-1α（HIF-1α）Bax and Bcl-2, and reveal the mechanism underlying the role of HIF-1α in hepatocyte apoptosis. Methods Sixty rats were divided randomly into the four groups: the normal control group, rats were treated normally; IH group, rats were treated by 30s nitrogen and then 90s air, which was called one cycle, and rats were treated by 120 cycle from nine clock to seventeen clock daily;pulmonary emphysema group, rats were treated by smudging, the condition of smudging was set for half an hour, twice a day (eight clock and sixteen clock); IH with pulmonary emphysema group, rats were treated by 120 cycle which were composed of 30s nitrogen and then 90s air from nine clock to seventeen clock daily. After exposed fourteen weeks, the whole rats were killed. qRT-PCR assay was conducted to detect the expression of HIF-1α mRNA, Bax mRNA, Bcl-2 mRNA in live tissues. Correlation analysis was applied to reveal the relationship between HIF-1α and Bax, Bcl-2. Results The expression of HIF-1α, Bax, Bax/Bcl-2 in IH with pulmonary emphysema group was significantly higher than that in other groups (P<0.05), and the expression of Bcl-2 in IH with pulmonary emphysema group was significantly lower than the pulmonary emphysema group and the normal control group, but the expression of Bcl-2 in IH with pulmonary emphysema group did not show significant difference compared with the IH group. Positive correlations existed between HIF-α and Bax, Bax/Bcl-2, while negative correlations existed between HIF-α and Bcl-2. Conclusion The expression of HIF-1α mRNA, Bax mRNA, Bcl-2 mRNA was induced in hepatocyte under the condition of intermittent hypoxia with pulmonary emphysema, and the induction was greater than that under purely intermittent hypoxia and pulmonary emphysema. HIF-1α expression correlated with Bax and Bcl-2, suggesting that HIF-1α may promote the hepatocyte apoptosis through transcriptional coactivators, Bax and Bcl-2.

Key words: HIF-1α, intermittent hypoxia, pulmonary emphysema, overlap syndrome, hepatocyte, apoptosis