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目的研究凉膈散对内毒(LPS)素诱导大鼠急性肺损伤(ALI)时Toll样受体4(TLR4)表达的影响。方法大鼠随机分成LPS组、LPS+3个不同剂量凉膈散组、LPS+地塞米松组、对照组,注射LPS后于1,2,4,8,16 h不同时相处死动物。采用蛋白免疫印迹分析(Western blot)法检测大鼠肺组织中TLR4蛋白表达的变化,光镜下观察肺组织病理学改变。结果与对照组比较,大鼠尾静脉注射LPS(5 mg.kg-1)后,LPS组大鼠肺组织TLR4表达开始增高,4 h达高峰(P<0.01),随后表达逐渐下降,到16 h时其表达仍高于对照组。与LPS组比较,凉膈散和地塞米松预处理组在2,4,8 h可显著降低TLR4的表达(P<0.05,P<0.01),凉膈散各组及地塞米松组各组间比较均无显著性差异。结论 TLR4在大鼠肺组织内广泛分布,LPS刺激可使TLR4的表达增加,凉膈散可抑制TLR4的增加,这可能是凉膈散抗内毒素急性肺损伤的机制之一。
Objective To investigate the effect of Liangge San on Toll-like Receptor 4 (TLR4) expression induced by lipopolysaccharide (LPS) -induced acute lung injury (ALI) in rats. Methods Rats were randomly divided into LPS group, LPS + three different doses of Liangge powder group, LPS + dexamethasone group, control group, and animals were sacrificed at different time points after 1,2,4,8,16 h injection of LPS. The changes of TLR4 protein expression in lung tissue were detected by Western blotting, and pathological changes of lung tissue were observed under light microscope. Results Compared with the control group, the TLR4 expression in the lung tissue of LPS group began to increase at the peak of 4 h after LPS injection (5 mg.kg-1) in tail vein of rats, reaching the peak at 4 h (P <0.01), and then gradually decreased to 16 h expression was still higher than the control group. Compared with LPS group, the rats in Liangge Powder group and dexamethasone group could significantly reduce the expression of TLR4 (P <0.05, P <0.01) at 2, 4 and 8 h, There was no significant difference between the two groups. Conclusion TLR4 is widely distributed in the lung tissue of rats. LPS stimulation can increase the expression of TLR4, and Lengge Powder can inhibit the increase of TLR4, which may be one of the mechanisms of Lengge San against endotoxin acute lung injury.