Objective To determine changes of angiotensin converting enzyme 2 (ACE2) in the development of chronic intermittent hypoxia (CIH)-induced pulmonary injury in rats and its mechanism. Methods 96 adult male Wistar rats were randomly allocated into four groups: control (UC) group, chronic intermittent hypoxia (CIH) group, normal saline treated CIH (NS) group, and edaravone treated CIH (NE) group. Each group contained four subgroups of rats (n=6) subjecting to 1 week, 2 weeks, 3 weeks, and 4 weeks experiment, respectively. No intervention was given to rats in the UC group. Rats in the experimental groups were exposed to alternating cycles of nitrogen and compressed air. Rats in the NS and NE groups received daily injection of 0.9% normal saline (3 mg/kg) and edaravone (3 mg/kg), respectively. Pulmonary sections were taken and stained with hematoxylin-eosin (HE). The levels of malondialdehyde (MDA), ACE2, ACE2mRNA, and angiotensin Ⅱ(AngⅡ) mRNA in the rat homogenate pulmonary samples were measured. Results Rats in the CIH and NS groups showed high levels of interstitial edema, alveolar atelectasis, and inflammatory cell infiltration in alveolar epithelial cells. The pulmonary injury got worse over time. Rats in the NE group showed later occurrence and milder pulmonary injury compared with those in the NS group. Rats in the CIH and NS groups had higher levels of and AngⅡ mRNA (which increased over time) than those in the UC group (PACE2 and the level of ACE2mRNA increased in rats in the CIH group (PPMDA andAngⅡ mRNA compared with those in the NS group(PACE2 and ACE2 mRNA compared with those in the UC and SC groups (PAngⅡmRNA was positively correlated with MDA(r=0.782, PAngⅡ, which maybe an important mechanism of CIH-induced pulmonary injury.
