Objective To study the effect of hypoxia on the expressions of interleukin-1β, 4, 10, and 13 (IL-1β, IL-4, IL-10 and IL-13) in pulmonary arterial smooth muscle cells (PASMCs) and the regulative role of cocultured pulmonary microvascular endothelial cells (PMVECs). Methods Rat PASMCs were cocultured with or without rat PMVECs, and randomly divided into 5 groups, normal group (N), 2-hour hypoxia (H2), 6-hour hypoxia (H6), 12-hour hypoxia (H12), and 24-hour hypoxia (H24). The expressions of IL-1β, IL-4, IL-10 and IL-13 in the supernatant were detected with ELISA. Results The expression levels of IL-1β, IL-4, IL-10 and IL-13 was increased in H2 group, peaked in H6 group, and then decreased in H12 group. However, the expression levels of above-mentioned cytokines in cocultured groups were significantly lower than those in corresponding hypoxia group. Conclusion Hypoxia can enhance activities of IL-1β, IL-4, IL-10, and IL-13 in PASMCs, but this enhancement can be down-regulated by cocultured PMVECs.

Objective To investigate the expression of heme oxygenase (HO) in pulmonary arteries of rats with hypoxic pulmonary hypertension (HPH). Methods A total of 60 rats were employed and equally divided into 5 groups (n=12 in each group) , i. e. control (group Ⅰ), HPH (group Ⅱ), hemin (group Ⅲ), tin protoporphyrin (SnPP) (group Ⅳ), and low concentration CO group (group Ⅴ). Of them, the rats from mid-dle 3 groups were treated with hypoxia under normal pressure for 7 h in every day except Sunday, consecutively for 3 weeks. Hemin and tin protoporphyrin (SnPP) were given half an hour before hypoxia while low concentra-tion CO at 2 h after hypoxia. HO-1 activity of pulmonary arteries tissues was tested with ultraviolet spectropho-tometry. The expression of HO was detected with reverse transcriptionpolymerase chain reaction (RT-PCR), immunohistochemical staining and in situ hybridization. Results ①The bilirubin production increased signifi-cantly in group [(396.28±69.62) pmol·mg-1·h-1], group [(668.56±189.29) pmol·mg-1·h-1], group [(267.38±88.59) pmol·mg-1·h-1]and group [(589.32±132.35) pmol·mg-1·h-1], as com-pared with those in group [(125.62±31.52) pmol·mg-1·h-1]. ②The levels of HO-1 mRNA expression of pulmonary arteries in group Ⅱ, group Ⅲ, group Ⅳ and group Ⅴ were significantly higher than those in group Ⅰ. The most significant HO-1 mRNA expression was found in group Ⅴ (P <0.01). The levels of HO-1 mRNA expression of pulmonary arteries in group Ⅲ and group Ⅴ were higher than those in group Ⅱ, but it was lower in group Ⅳ than that in group Ⅱ. ③The strong positive granules of HO-1 were observed in pulmonary arteries intima and media in group Ⅱ, group Ⅲ and group Ⅳ, while group Ⅲ and group Ⅳ involved more pos-itive granules of HO-1 as compared with those in group Ⅱ. ④The staining was deepened in three layers of the pulmonary arteries in group Ⅱ, while the staining was deepened more in group Ⅲ and group Ⅳ. No significant change was found in staining of HO-2 in different groups. Conclusion CO can up-regulate the expression of HO-1, and this may play important roles in the genesis and development of pulmonary hypertension.