Objective The aim of present study was to observe the expression of MK2 and HuR in mice with lipopolysaccharide (LPS) - induced acute lung injury. Methods Mice with acute lung injury induced by LPS was successfully reproduced. We observed pathological in lung tissue, and wet/ dry weight (W/D) , immunohischemistry method was used to determine MK2 and HuR protein levels, and western bolt was used to test protein expression in cytoplasm and nucleus and phosphorylation of MK2. Results Alveolar edema was observed in the LPS group, wet/dry weight ratio was higher than those in normal control group, and it matched the characteristics of ALI. Protein expression of MK2 is little in normal lung tissue, and the total protein of MK2 after LPS stimulation did not change significantly in lung tissue, but phosphorylated MK2 increased greatly. The expression of HuR did not change obviously between the control group and the LPS group, while protein expression of HuR increased in the cytoplasm. Conclusion Both MK2 and HuR, which were phosphorylated and translocated respectively, have participated in the ALI.%目的 在脂多糖(LPS)复制的急性肺损伤(ALI)小鼠模型中,观察MK2和HuR在ALI发病中的表达变化.方法 在LPS复制的小鼠ALI模型中观察肺组织病理、湿/干重比(W/D),并用免疫组化观察肺组织MK2和HuR的改变,同时用Western bolt法检测总MK2和磷酸化MK2、HuR总蛋白和细胞质、细胞核中HuR表达量的变化.结果 ALI小鼠肺组织病理显示肺组织受损,W/D增加,符合ALI表现.正常小鼠肺组织表达MK2量较少,LPS刺激后肺组织中MK2表达总量无明显变化,而磷酸化MK2明显增加.HuR在正常组和肺损伤组小鼠肺组织中表达总量无明显变化,但在损伤组细胞质中表达量明显增加.结论 MK2磷酸化和HuR亚细胞定位改变可能参与ALI反应.
展开▼
