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目的探讨胎盘TLR2受体的表达与子痫前期发病机制的相关性。方法通过免疫组化法及Western印迹法比较早发型子痫前期组、早发型对照组、晚发型子痫前期组及晚发型对照组的胎盘TLR2的表达,探讨TLR2的表达与子痫前期的发病机制相关性。结果早发型子痫前期组胎盘TLR2受体的表达量比早发型对照组显著增高,也比晚发型子痫前期组显著增高,差异均有统计学意义(P<0.05),晚发型子痫前期组与晚发型对照组之间TLR2的表达量差异无统计学意义(P>0.05)。结论早发型子痫前期与晚发型子痫前期的发病机制可能不同,炎症免疫过度激活可能是早发型子痫前期的主要发病机制,TLR2是重要的免疫调节因子。
Objective To investigate the relationship between placental TLR2 receptor expression and the pathogenesis of preeclampsia. Methods The expression of TLR2 in placenta of early-onset preeclampsia group, early-onset preeclampsia group, late-onset preeclampsia group and late-onset preeclampsia group were compared by immunohistochemistry and Western blotting to explore the relationship between TLR2 expression and preeclampsia Mechanism relatedness. Results The expression of placental TLR2 receptor in preeclampsia group was significantly higher than that in the early onset preeclampsia group and also significantly higher than that in the late onset preeclampsia group (P <0.05). The incidence of late onset preeclampsia There was no significant difference in TLR2 expression between the two groups (P> 0.05). Conclusion The pathogenesis of preeclampsia and late onset preeclampsia may be different. The over-activation of inflammation may be the main pathogenesis of preeclampsia. TLR2 is an important immunoregulatory factor.