The protective effect of high heme oxygenase-1 expression induced by propofol on the alveolar II type epithelial cells of rats with acute lung injury induced by oleic acid.

This study aimed to investigate the mechanism of propofol (PR) pretreatment inducing high heme oxygenase-1 (HO-1) expression to protect alveolar type II epithelial cells (AEC-II) in rats with acute lung injury (ALI) induced by oleic acid (OA). In this study, 32 male Sprague-Dawley rats (250 - 300 g) were randomly divided into four groups (n = 8 in each group) as follows: group C (the normal control group), the OA group (the oleic acid injury control group), the OA + PR group (the PR pretreatment group), and the OA + IX group (the zinc porphyrin IX pretreatment group). Arterial blood gases, bronchoalveolar lavage fluid (BALF), and serum pulmonary surfactant-associated protein A (SP-A) were measured in each group. The changes in the AEC-II ultrastructure were observed under an electron microscope. The HO-1 protein expression was detected by immunohistochemistry, and HO-1 messenger ribonucleic acid (mRNA) was detected by polymerase chain reaction. The results of this study showed that there were significant differences in PO ₂ , pCO ₂ , and PaO ₂ /FiO ₂ among the different groups (p < 0.05). The difference between BALF and SP-A in each group was statistically significant (p < 0.01). There were also significant differences in the integrated optical density of the HO-1 protein expression and HO-1 mRNA in the pulmonary tissue of the different groups (p < 0.05 or p < 0.01). The results of the electron microscopy showed that AEC-II were relatively irregular in the OA group. The cells degenerated and even disintegrated, the microvilli on the cell surface decreased, the lamellar bodies in the cytoplasm were evacuated, and some were discharged into the alveolar cavity. The above-mentioned changes in the OA + PR group were lower than in the OA group, while the changes were greater in the OA + IX group, compared with those in the OA group. We conclude that PR can significantly increase the expression of HO-1 in pulmonary tissues and reduce pulmonary injury, and, therefore, protect the AEC-II.