目的：观察急性肺损伤(acute lung injury，ALI)小鼠肺内热休克蛋白A12B( heat shock protein A12B，HSPA12B)的表达改变，以及脂多糖(lipopolysaccharide，LPS)对血管内皮细胞HSPA12B表达的影响。方法：采用气管注射LPS(5 mg/kg)复制小鼠ALI动物模型，6 h后取小鼠肺组织，采用real-time PCR和Western印迹检测肺组织内HSPA12B mRNA和蛋白表达。体外研究采用LPS (1 μg/mL)诱导人脐静脉内皮细胞炎症反应，real-time PCR和Western印迹检测细胞HSPA12B mRNA和蛋白表达，采用NF-κB信号通路抑制剂PDTC观察LPS诱导HSPA12B表达的可能分子机制。结果：与正常组相比，LPS诱导的ALI小鼠肺组织HSPA12B mRNA和蛋白含量显著增加，同时LPS可时间依赖性地上调人脐静脉内皮细胞HSPA12B mRNA和蛋白表达，而PDTC预处理可部分逆转LPS诱导的HSPA12B mRNA和蛋白上调。结论：ALI小鼠肺内HSPA12B的表达增加，其机制可能与LPS激活NF-κB信号通路有关。
Expression of HSPA12B in lung of acute lung injury mice
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 significantly increased. The 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 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.