环氧合酶2及前列腺素15-羟基脱氢酶在早产患者胎盘及胎膜组织中的表达

目的探讨环氧合酶2(COX-2)、前列腺素15-羟基脱氢酶(15-PGDH)在胎盘和胎膜组织中的表达变化及其与早产发生的关系。方法采用免疫组化二步法,测定14例早产产妇(早产组)、18例足月临产产妇(足月临产组)、17例足月未临产产妇(对照组)的胎盘和胎膜组织中COX-2与15-PGDH的定位与表达水平(以阳性百分数计分和细胞染色计分相加表示)。结果(1)COX-2在3组产妇的羊膜上皮细胞、绒毛膜细胞和蜕膜细胞的胞质中均有表达。COX-2在早产组胎膜和胎盘组织羊膜上皮细胞中的表达水平分别为(4·6±1·2)、(4·7±0·9)分,在足月临产组分别为(3·2±1·0)、(3·6±1·0)分,在对照组分别为(2·2±0·6)、(2·5±0·9)分。早产组及足月临产组明显高于对照组,两两比较,差异均有统计学意义(P<0·01);早产组与足月临产组比较,差异也有统计学意义(P<0·01)。3组间胎膜羊膜上皮细胞与胎盘羊膜上皮细胞中的COX-2表达水平相互比较,差异均无统计学意义(P>0·05)。(2)COX-2在早产组胎盘绒毛膜细胞中的表达水平为(4·9±1·0)分,在足月临产组为(3·9±1·2)分,在对照组为(2·3±0·7)分,早产组及足月临产组明显高于对照组,两两比较,差异均有统计学意义(P<0·01);早产组与足月临产组比较,差异也有统计学意义(P<0·01)。而3组胎膜绒毛膜组织中COX-2表达水平比较,差异无统计学意义(P>0·05);在3组胎盘蜕膜细胞中的表达水平比较,差异也无统计学意义(P>0·05)。(3)15-PGDH在3组产妇羊膜上皮细胞、绒毛膜细胞和蜕膜细胞的胞质中均有表达,3组胎膜及胎盘组织的羊膜上皮细胞中15-PGDH表达水平比较,差异无统计学意义(P>0·05);而在胎膜及胎盘组织的绒毛膜细胞中表达水平,早产组分别为(1·5±0·6)、(2·3±0·8)分,足月临产组分别为(2·6±0·8)、(3·0±0·7)分,对照组分别为(4·4±1·1)、(4·1±1·2)分,早产组及足月临产组明显低于对照组,两者比较,差异有统计学意义(P<0·01);早产组与足月临产组比较,差异也有统计学意义(P<0·05)。在胎盘组织蜕膜细胞中的表达水平,早产组为(2·1±0·7)分,足月临产组为(2·8±0·8)分,对照组为(4·5±1·0)分,早产组及足月临产组明显低于对照组,两者比较,差异有统计学意义(P<0·01);早产组与足月临产组比较,差异也有统计学意义(P<0·05)。结论COX-2在羊膜上皮细胞中的高表达和15-PGDH在绒毛膜、蜕膜细胞中的低表达,与早产的分娩发动有关。二者在早产的发生中起一定作用。

Expression of cyclooxygenase-2 and 15-prostaglandin dehydrogenase of placenta and fetal membranes in patients of preterm labor

OBJECTIVE: To investigate the effect of cyclooxygenase 2 (COX-2) and 15-prostaglandin dehydrogenase (15-PGDH) on preterm labor. METHODS: The expressions and localizations of COX-2 and 15-PGDH in placentas and fetal membranes were examined by immunohistochemical (IH) two-step assay (IH scores were expressed as the sum of the percentage of immunoreactivity and the stained degree of cells), respectively. The samples were obtained from 14 preterm delivery (PL), 18 term in labor (TL) and 17 term not in labor (control group). RESULTS: (1) The immunoreactivity of COX-2 was found in the amniotic epithelial cells, chorion cells and decidual cells. IH scores of COX-2 in amniotic epithelium of placenta or fetal membranes in PL were 4.6 +/- 1.2, 4.7 +/- 0.9, respectively; in TL were 3.2 +/- 1.0, 3.6 +/- 1.0, respectively, and in control group were 2.2 +/- 0.6, 2.5 +/- 0.9, respectively. IH scores in PL and TL were obviously higher than those in control group (P < 0.01). It was higher in PL than in TL (P < 0.01). The expression of COX-2 was not significantly different between amnion of placenta and amnion of fetal membranes among the three groups (P > 0.05). (2) IH scores of COX-2 in chorion of placenta in PL were 4.9 +/- 1.0, in TL were 3.9 +/- 1.2 and in control group were 2.3 +/- 0.7. IH scores in PL and TL were obviously higher than those in control group (P < 0.01), and it was higher in PL than in TL (P < 0.01). The expression of COX-2 was not significantly different among the three groups in chorion of fetal membranes (P > 0.05) and it was not significantly different among the three groups in decidual cell of placenta (P > 0.05), either. (3) The immunoreactivity of 15-PGDH was found in the amniotic epithelial cells, chorion cells and decidual cells. The expression of 15-PGDH was not significantly different among the three groups in amnion of placenta or fetal membranes (P > 0.05). IH scores of 15-PGDH in chorion of placenta and fetal membranes in PL were 1.5 +/- 0.6, 2.3 +/- 0.8, respectively, in TL were 2.6 +/- 0.8, 3.0 +/- 0.7, respectively, and in control group were 4.4 +/- 1.1, 4.1 +/- 1.2, respectively. IH scores in PL and TL were obviously lower than those in control group (P < 0.01), and it was lower in PL than in TL (P < 0.05). IH scores of 15-PGDH in decidua of placenta in PL were 2.1 +/- 0.7, in TL were 2.8 +/- 0.8 and in control group were 4.5 +/- 1.0. IH scores in PL and TL were obviously lower than those in control group (P < 0.01); it was lower in PL than in TL (P < 0.05). CONCLUSIONS: The higher expression of COX-2 in amniotic epithelium and the lower expression of 15-PGDH in chorion and decidual cell are relevant with the onset of premature labor. They play a role in the pathogenesis of premature labor.