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目的研究子前期(PE)患者胎盘组织中Toll样受体2(TLR2)和Toll样受体4(TLR4)的表达及其与胎盘中肿瘤坏死因子α(TNF-α)、白介素6(IL-6)表达的关系,探讨PE胎盘中Toll样受体变化的意义。方法2005年1月至2006年12月在哈尔滨医科大学第一临床医学院采用免疫组化和RT-PCR法检测PE患者和正常晚期妊娠妇女胎盘组织中TLR2和TLR4的定位及表达,同时用脂多糖(LPS)体外刺激胎盘组织中的TLR4,检测其上清液中TNF-α、IL-6的变化。其中PE患者44例(PE组),同期正常晚期妊娠妇女22例(对照组)。结果PE组和对照组胎盘组织中均有TLR2和TLR4的表达,其中PE组TLR4表达明显比对照组增强,组间差异有显著性意义(P<0.05);LPS体外刺激PE组胎盘组织,导致TNF-α、IL-6分泌量增加,刺激后2hPE组TNF-α、IL-6分泌量与对照组比较差异无显著意义(P>0.05),刺激后6hPE组TNF-α、IL-6的分泌量升高明显,与对照组比较,差异有显著性意义(P<0.01)。结论PE患者胎盘中TLR4表达增加与TNF-α、IL-6改变密切相关,是造成局部细胞因子微环境异常的主要因素,其增加可能是PE发病机制中的关键环节之一。
Objective To investigate the expression of Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) in the placenta of preeclampsia (PE) and its relationship with the expression of tumor necrosis factor-α (TNF- -6), and to explore the significance of Toll-like receptors in PE placenta. Methods From January 2005 to December 2006, the localization and expression of TLR2 and TLR4 in placenta of PE patients and normal pregnant women were detected by immunohistochemistry and RT-PCR in Harbin Medical University No.1 School of Clinical Medicine. At the same time, Polysaccharides (LPS) stimulated TLR4 in placenta in vitro and detected the changes of TNF-α and IL-6 in supernatant. There were 44 PE patients (PE group) and 22 normal pregnant women in the same period (control group). Results The expression of TLR2 and TLR4 in both placental tissue of PE group and control group were significantly higher than that of control group (P <0.05). LPS stimulation of placental tissue in PE group resulted in The secretion of TNF-αand IL-6 increased at 2 h after stimulation, while the secretion of TNF-α and IL-6 at 2 hPE after stimulation had no significant difference compared with the control group (P> 0.05) Secretion increased significantly, compared with the control group, the difference was significant (P <0.01). Conclusions The increased expression of TLR4 in placenta of PE patients is closely related to the changes of TNF-α and IL-6, which is one of the main factors that cause abnormalities of local cytokine microenvironment. The increase may be one of the key links in the pathogenesis of PE.