脂多糖对小鼠子宫内膜Toll样受体4介导的炎性信号通路的影响

Effect of LPS on inflammatory signal pathway mediated by TLR4 in endometrium of mice

革兰阴性菌感染可引起子宫内膜炎,机体的Toll样受体4(TLR4)可接受革兰阴性菌的细胞壁主要成分脂多糖(LPS)的刺激引发一系列炎症反应。为了研究LPS对TLR4介导的炎性信号通路的影响,本试验以小鼠为模型,分别用不同浓度的LPS对小鼠进行在体子宫灌注和处理体外培养的子宫内膜上皮细胞系。组织学观察显示,灌注不同浓度LPS后子宫内膜组织中炎性细胞增多。通过RT-PCR对各组中TLR4和核转录因子κB(NF-κB)、IL-6的mRNA表达水平进行检测,发现LPS刺激能够增强TLR4和NF-κB、IL-6 mRNA表达,影响TLR4介导的炎性信号通路。

Gram-negative bacteria are leading cause of endometritis. Lipopolysaccharide （LPS）, which is main component of cell wall of Gram-negative bacteria, can stimulate inflammation responses. In order to investigate the effect of LPS on Toll-like receptor 4 （TLR4） -me- diated inflammatory signaling pathway, this experiment was conducted in mice. Infusion was taken to mice uterine in vivo and LPS was added to endometrial epithelial cell culture in vitro with different concentration of LPS, respectively. Histological observation showed that after infu- sion with LPS, the inflammatory cells in endometrial tissue increased. The RT-PCR results showed that LPS stimulation could increase TLR4, nuclear factor kappa B （NF-KB） and IL-6 mRNA expression levels, indicating its effect on TLR4-mediated inflammatory signaling pathway.