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目的探讨Sonic hedgehog(SHH)信号通路中Shh、Gli1及核因子-κB(nuclear factor kappa B,NF-κB)在脂多糖诱导的小鼠急性肺损伤中的表达变化。方法脂多糖腹腔注射复制小鼠急性肺损伤模型,实验动物随机分为实验组(脂多糖5 mg/kg)和对照组。分别于给药后6、12、24 h取肺组织,观察肺组织病理改变、肺湿干重比值(W/D)、RT-PCR和Western blot检测Shh、Gli1的m RNA和蛋白表达,Western blot检测NF-κB的蛋白表达。结果实验组肺组织病理损伤评分及W/D比值明显高于对照组(P<0.05)。Shh的m RNA表达水平在各时间点均高于对照组(P<0.05),且与时间呈正相关(P<0.01)。6 h时Gli1的m RNA表达水平与对照组无明显差异(P>0.05),12、24 h时明显高于对照组(P<0.01),且与时间呈正相关(P<0.01)。与对照组相比,实验组6、12、24 h时Shh、Gli1的蛋白表达水平均明显升高(P<0.05),且与时间呈正相关(P<0.01)。NF-κB的蛋白表达在各时间点均明显高于对照组(P<0.05)。结论脂多糖诱导的小鼠急性肺损伤中Shh、Gli1表达上调可能是脂多糖通过调控NF-κB来实现的。
Objective To investigate the expression changes of Shh, Gli1 and nuclear factor kappa B (NF-κB) in the Sonic hedgehog (SHH) signaling pathway in mice with acute lung injury induced by lipopolysaccharide. Methods Lipopolysaccharide was intraperitoneally injected into a mouse model of acute lung injury. The experimental animals were randomly divided into experimental group (lipopolysaccharide 5 mg / kg) and control group. The lung tissues were taken at 6, 12, and 24 h after administration, respectively. The pathological changes of lung tissue and W / D ratio were observed. The mRNA and protein expressions of Shh and Gli1 were detected by RT-PCR and Western blot, blot detection of NF-κB protein expression. Results The histopathological damage score and W / D ratio in experimental group were significantly higher than those in control group (P <0.05). The expression of m RNA in Shh was higher than that in control group at each time point (P <0.05), and positively correlated with time (P <0.01). At 6 h, the expression of m RNA in Gli1 was not significantly different from that in control group (P> 0.05), but significantly higher than that in control group at 12 and 24 h (P <0.01). Compared with the control group, the protein expression levels of Shh and Gli1 in experimental group were significantly increased at 6, 12, 24 h (P <0.05), and positively correlated with the time (P <0.01). The protein expression of NF-κB at each time point was significantly higher than that of the control group (P <0.05). Conclusion Upregulation of Shh and Gli1 in LPS-induced acute lung injury may be caused by the regulation of lipopolysaccharide by regulating NF-κB.