Objective To investigate the role and mechanism of silent information regulator 1 (SIRT1) on type Ⅱ alveolar epithelial cell injury in lipopolysaccharide (LPS) induced rats.

Methods Primary type Ⅱ alveolar epithelial cells were isolated from rats and divided into control group, model group and experimental group. Model group and experimental group were infected with blank and SIRT1 shRNA lentivirus respectively, and then LPS was added to induce cell injury. The expression of SIRT1 was detected by real-time quantitative polymerase chain reaction (PCR) and Western blot; the cell viability was detected by CCK-8 assay; the expressions of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were detected by real-time quantitative PCR and enzyme-linked immunosorbent assay (ELISA); the mitochondrial membrane potential was detected by JC-1 staining assay; the level of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) were detected by chemical chromogenic assay.

Results Compared with the control group, SIRT1 mRNA and protein expression levels of type Ⅱ alveolar epithelial cells in the model group increased significantly, cell viability decreased significantly, mRNA expression levels and secretion levels of pro-inflammatory factors such as TNF-α and IL-1β increased significantly, mitochondrial membrane potential decreased significantly, MDA level increased significantly, and SOD activity decreased significantly (P < 0.05). Compared with the model group, SIRT1 mRNA and protein expression levels of type Ⅱ alveolar epithelial cells in the experimental group decreased significantly, cell viability increased significantly, mRNA expression levels and secretion levels of pro-inflammatory factors such as TNF-α and IL-1β decreased significantly, mitochondrial membrane potential increased significantly, MDA level decreased significantly, and SOD activity increased significantly (P < 0.05).

Conclusion SIRT1 can promote LPS-induced type Ⅱ alveolar epithelial cell injury by affecting mitochondrial activity and cell redox homeostasis.