Objective: To observe the expression of heat shock protein A12B (HSPA12B) in lungs of acute lung injury (ALI) mice and the effect of lipopolysaccharide (LPS) on the expression of HSPA12B in vascular endothelial cells. Methods: Mouse was injected with LPS (5 mg/kg), and lung tissue was taken at 6 h. The expression of HSPA12B mRNA and protein in lung tissue was detected by real-time PCR and Western blot. In vitro, human umbilical vein endothelial cells were stimulated by LPS (1 μg/mL). Real-time PCR and Western blot were used to detect the expression of HSPA12B mRNA and protein. NF-κB signaling pathway inhibitor PDTC was used to observe the possible molecular mechanisms of LPS-induced HSPA12B expression. Results: Compared with the normal group, the expression of HSPA12B mRNA and protein in LPS-induced lung tissue of ALI mice were signi cantly increased. e expression of HSPA12B mRNA and protein in human umbilical vein endothelial cells were up-regulated in a time-dependent manner. NF-κB inhibitor (PDTC) pretreatment reversed the LPS-induced
2017, 37(8) h p://lcbl.amegroups.com HSPA12B mRNA and protein upregulation. Conclusion: The expression of HSPA12B in lung of ALI mice
increases, and its mechanism is related to the activation of NF-κB signaling pathway.