重度子痫前期患者胎盘组织缺氧适应相关基因的表达及意义

 目的探讨重度子痫前期患者胎盘组织中缺氧适应相关基因HIF-1α、PHD1、PHD2和FIH-1的表达及意义。方法采
用免疫组化方法检测34 例重度子痫前期患者和24 例正常孕妇的胎盘组织中的HIF-1α、PHD1、PHD 2和FIH-1 蛋白的表达，
对两组的表达水平进行比较分析。结果在重度子痫前期患者和正常孕妇的胎盘组织中HIF-1α、PHD1、PHD 2和FIH-1蛋白
均主要表达在合体滋养细胞和细胞滋养细胞的胞浆中。重度子痫前期组HIF-1α和PHD 2蛋白表达（+++）者分别为16 例
（16/34）和14 例（14/34），显著高于对照组2 例（2/24）和2 例（2/24），差异均有统计学意义（ 约0.01）。PHD1 和FIH-1 蛋白在重
度子痫前期组中表达（+++）者分别是2 例（2/34）和2 例（2/34），明显低于对照组14 例（14/24）和13 例（13/24），2 组比较，差异均
有统计学意义（ P<0.01）。结论HIF-1α和PHD2 的蛋白在重度子痫前期患者胎盘组织中表达水平明显增高；而PHD1 和
FIH-1 的蛋白的表达水平却明显降低。PHD1、PHD2 和FIH-1 可能通过抑制HIF-1α的机制参与重度子痫前期的发病。

Expressions and Significations of Hypoxic-adjusting Related Genes in Placenta of Severe Preeclampsia

Objective To investigate the expressions and significations of HIF-1α，PHD1，PHD2 and FIH-1 in the placentas of women
with severe preeclampsia. Methods Placentas were collected from 34 pregnant women with severe preeclampsia as study group and from
24 normal pregnant women as control group. The expressions of HIF-1α，PHD1，PHD2 and FIH-1 proteins were semi-quantitatively analyzed
with immunohistochemical assay. Results The HIF-1α，PHD1，PHD2 and FIH-1 protein were all mainly distributed in the cytoplasm of
syncytiotrophoblasts and cytotrophoblasts in the placentas of patients with severe preeclampsia and normal pregnant women. The strong posi-
tive（+++）expressions of HIF-1αand PHD2 proteins were observed in 16 cases （16/34）and 14 cases（14/34）respectively in severe
preeclampsia group，significantly higher than control group （2 cases，2/24 and 2 cases，2/24）. （ P<0.01， P<0.01）. The strong positive
（+++）expressions of PHD1 and FIH-1 proteins were observed in 2 cases and 2 cases（2/34，2/34）respectively in severe preeclampsia
group，significantly lower than those in control group（14 cases，14/24 and 13 cases，13/24）.（ P<0.01， P<0.01）. Conclusion Compared
with the control group，expressions of HIF-1αand PHD2 are significantly higher and those of PHD1and FIH-1 are significantly lower in pla-
centas of patients with severe preeclampsia. PHD1，PHD2 and FIH-1 might play an important role in the pathogenesis of preeclampsia
through inhibition of HIF-1αby a complex mechanism.