Abstract: Objective To investigate the effects of heat shock protein A12A (HSPA12A) on lung injury during endotoxemia. Methods HSPA12A knockout mice (Hspa12a^-/-) and wild type littermates (WT) mice aged 8-10 weeks were enrolled in this study. The mice were injected with lipopolysaccharide (LPS) intraperitoneally to induce endotoxemia, while normal saline (NS)-treated mice served as the controls. According to the type of mice and treatment mode, the mice were divided into NS-WT group, NS-Hspa12a^-/- group, LPS-WT group and LPS-Hspa12a^-/- group. Six hours after LPS or NS treatment, the lung tissues were harvested for the detection of protein levels and paraffin sections. The arterial blood was collected for arterial blood gas analysis. Protein expression levels were detected by immunoblotting. Pulmonary injury scores were obtained according to the histopathological changes of the lung tissues by H&E staining, and the pulmonary function was evaluated by blood gas analysis. Results The expression level of HSPA12A in the lungs of LPS-treated mice was 150% of that in NS-treated mice (P<0.05). After LPS treatment, the lung tissues showed obvious pathological changes, and Hspa12a^-/- mice showed severer pulmonary histological abnormalities and higher injury scores than those in WT mice (P<0.01). Hspa12a^-/- mice showed increased CO₂ accumulation in arterial blood than WT mice during endotoxemia (P<0.05). Conclusions HSPA12A plays an important role in the protection against sepsis/septic shock-induced lung injury.

Key words: heat shock protern A12A, endotoxemia, lung injury