Abstract: Objective To explore the effect and mechanism of miR-322 on the occurrence and development of pulmonary hypertension at high altitude. Methods Forty SPF male rats were randomly divided into 4 groups (n=10): normoxic group (Normoxia), hypoxia group (Hypoxia), blank virus + hypoxia group (no load group) and miR-322 inhibition + hypoxia group (miR-322 group). The dead rats during the experiment were excluded, and eventually there were 10 rats in normoxic group, 9 rats in hypoxia group, empty load group and miR-322 group respectively. The pulmonary arterial oxygen partial pressure [p (O2)] and mean pulmonary artery pressure (mPAP) were measured. HE staining was used to observe the changes of lung tissue. The expression of α-SMA was observed by immunofluorescence. miR-322 and apelin mRNA gene expressions in rat lung tissues were detected by real-time PCR. The expression of apelin protein in rat lung tissue was detected by Western blot assay. Results There were no significant differences in p (O2), mPAP and indicators of lung tissues between hypoxia group and no-load group. Compared with the normoxic group, the relative expressions of mPAP, α- SMA, apelin protein and miR-322 were increased, and p (O2) was decreased in the hypoxia group (P＜0.05). The lung tissues were severely damaged and a large number of inflammatory cells infiltrated. Compared with hypoxia group, the relative expressions of mPAP and miR-322 were decreased in miR-322 group, the p (O2) in pulmonary artery and the relative expression of apelin protein increased, α-SMA and lung tissue damage decreased (P＜0.05). Conclusion The inhibition of miR-322 expression promotes the expression of apelin in rats with high altitude pulmonary hypertension and reduces the rise of high altitude pulmonary hypertension.

Key words: hypertension, pulmonary, altitude sickness, disease models, animal, miR-322, apelin