Dimitrakova E, Milchev N, Batashki I, Karumanchi S A
Akush Ginekol (Sofiia). 2007;46(9):4-8.
The object of the present study was to cause-effect relationships between serum placental angiogenic proteins and IL-2, IL-6, IL-10 levels in pregnant women with preeclampsia.
We studied a total of 70 women, aget 18-36/25+/-4.1/40 women had preeclampsia, 30 had normal pregnancies and 30 women were healthy controls. We measured the serm levels of fms-like tyrosine kinase-1, placental growth factor (PLGF), IL-2, IL-6, IL-10 using ELISA.
sFlt-1 serum levels were significantly higher and PLGF levels were significantly lower in women with preeclampsia as compare to those of healthy Pregnant women Likewise, IL-2, IL-6 levels were significantly higher in women with preeclampsia as compared to those of healthy pregnant women. IL-10 levels were not different between the two groups, sFlt-1, IL-2 and IL-6 were strongly correlated, PLGF and IL-2 were moderately correlated and there was no correlation with IL-10. There was a significant negative correlation between the two growth factors.
The abnormal balance of circulating angiogenic factors is a major pathgenetic mechanism underlying the endothelial dysfunction and clinical manifestations of preeclampsia. Endothelial dysfunction activated the expression and production of IL-2, and IL-6. The correlation of sFlt-1 and PLGF on one hand, and IL-2 and IL-6, on the other, is probably an factor which supports the participation of angiogenic proteins and cytokines in the pathogenesis of preeclampsia.
本研究的目的是探讨子痫前期孕妇血清胎盘血管生成蛋白与白细胞介素-2(IL-2)、白细胞介素-6(IL-6)、白细胞介素-10水平之间的因果关系。
我们共研究了70名女性,年龄18 - 36岁/平均年龄25±4.1岁,其中40名患有子痫前期,30名妊娠正常,30名作为健康对照。我们使用酶联免疫吸附测定法(ELISA)测量血清中类fms样酪氨酸激酶-1、胎盘生长因子(PLGF)、IL-2、IL-6、IL-10的水平。
与健康孕妇相比,子痫前期女性的可溶性fms样酪氨酸激酶-1(sFlt-1)血清水平显著升高,PLGF水平显著降低。同样,与健康孕妇相比,子痫前期女性的IL-2、IL-6水平显著升高。两组之间IL-10水平无差异,sFlt-1、IL-2和IL-6之间呈强相关,PLGF和IL-2呈中度相关,与IL-10无相关性。两种生长因子之间存在显著负相关。
循环血管生成因子的异常平衡是子痫前期内皮功能障碍和临床表现的主要发病机制。内皮功能障碍激活了IL-2和IL-6的表达与产生。一方面sFlt-1与PLGF,另一方面IL-2与IL-6之间的相关性可能是支持血管生成蛋白和细胞因子参与子痫前期发病机制的一个因素。