中华妇产科杂志
中華婦產科雜誌
중화부산과잡지
CHINESE JOUNAL OF OBSTETRICS AND GYNECOLOGY
2001年
2期
72-75
,共4页
程忠平%林其德%刘伟%陈珠萍%汪希鹏%沈仲毅
程忠平%林其德%劉偉%陳珠萍%汪希鵬%瀋仲毅
정충평%림기덕%류위%진주평%왕희붕%침중의
妊娠并发症,心血管%高血压%内皮生长因子%淋巴因子
妊娠併髮癥,心血管%高血壓%內皮生長因子%淋巴因子
임신병발증,심혈관%고혈압%내피생장인자%림파인자
目的探讨血管内皮生长因子(VEGF)与妊娠高血压综合征(妊高征)发病的相关性。方法采用酶联免疫吸附法检测23例妊高征患者(妊高征组)外周血及其新生儿脐静脉血VEGF水平,定量免疫组化及定量逆转录聚合酶链反应检测患者胎盘和蜕膜组织中VEGF表达情况,并以20例健康孕妇(正常妊娠组)为对照。结果(1)妊高征组外周血VEGF水平为[(10.4±3.8) ng/L,±s,下同],明显低于正常妊娠组的(17.0±9.3) ng/L。(2)胎盘合体滋养细胞及蜕膜间质滋养细胞均有VEGF强阳性染色。经计算机扫描图像处理,正常妊娠组绒毛合体滋养细胞VEGF表达为(75.0±9.0)平均灰度,间质细胞为(60.5±6.4)平均灰度,均显著高于妊高征组的(69.0±8.9)平均灰度和(55.0±7.3)平均灰度。正常妊娠组VEGF表达为(45.4±4.0) 平均灰度,显著高于妊高征组的(42.5±3.8) 平均灰度。(3)胎盘、蜕膜组织均有3种不同片断长度的VEGF mRNA扩增,正常妊娠组胎盘组织VEGF总峰度比为2.8±1.0,较妊高征组(4.6±3.2)极明显降低(P<0.01)。正常妊娠组蜕膜组织VEGF总峰度比为3.9±1.5,也较妊高征组(6.3±2.9)极明显降低,(P<0.01)。结论妊高征患者VEGF表达障碍发生在蛋白质翻译和表达水平;VEGF的异常表达在妊高征胎盘缺氧中具有重要的作用。
目的探討血管內皮生長因子(VEGF)與妊娠高血壓綜閤徵(妊高徵)髮病的相關性。方法採用酶聯免疫吸附法檢測23例妊高徵患者(妊高徵組)外週血及其新生兒臍靜脈血VEGF水平,定量免疫組化及定量逆轉錄聚閤酶鏈反應檢測患者胎盤和蛻膜組織中VEGF錶達情況,併以20例健康孕婦(正常妊娠組)為對照。結果(1)妊高徵組外週血VEGF水平為[(10.4±3.8) ng/L,±s,下同],明顯低于正常妊娠組的(17.0±9.3) ng/L。(2)胎盤閤體滋養細胞及蛻膜間質滋養細胞均有VEGF彊暘性染色。經計算機掃描圖像處理,正常妊娠組絨毛閤體滋養細胞VEGF錶達為(75.0±9.0)平均灰度,間質細胞為(60.5±6.4)平均灰度,均顯著高于妊高徵組的(69.0±8.9)平均灰度和(55.0±7.3)平均灰度。正常妊娠組VEGF錶達為(45.4±4.0) 平均灰度,顯著高于妊高徵組的(42.5±3.8) 平均灰度。(3)胎盤、蛻膜組織均有3種不同片斷長度的VEGF mRNA擴增,正常妊娠組胎盤組織VEGF總峰度比為2.8±1.0,較妊高徵組(4.6±3.2)極明顯降低(P<0.01)。正常妊娠組蛻膜組織VEGF總峰度比為3.9±1.5,也較妊高徵組(6.3±2.9)極明顯降低,(P<0.01)。結論妊高徵患者VEGF錶達障礙髮生在蛋白質翻譯和錶達水平;VEGF的異常錶達在妊高徵胎盤缺氧中具有重要的作用。
목적탐토혈관내피생장인자(VEGF)여임신고혈압종합정(임고정)발병적상관성。방법채용매련면역흡부법검측23례임고정환자(임고정조)외주혈급기신생인제정맥혈VEGF수평,정량면역조화급정량역전록취합매련반응검측환자태반화세막조직중VEGF표체정황,병이20례건강잉부(정상임신조)위대조。결과(1)임고정조외주혈VEGF수평위[(10.4±3.8) ng/L,±s,하동],명현저우정상임신조적(17.0±9.3) ng/L。(2)태반합체자양세포급세막간질자양세포균유VEGF강양성염색。경계산궤소묘도상처리,정상임신조융모합체자양세포VEGF표체위(75.0±9.0)평균회도,간질세포위(60.5±6.4)평균회도,균현저고우임고정조적(69.0±8.9)평균회도화(55.0±7.3)평균회도。정상임신조VEGF표체위(45.4±4.0) 평균회도,현저고우임고정조적(42.5±3.8) 평균회도。(3)태반、세막조직균유3충불동편단장도적VEGF mRNA확증,정상임신조태반조직VEGF총봉도비위2.8±1.0,교임고정조(4.6±3.2)겁명현강저(P<0.01)。정상임신조세막조직VEGF총봉도비위3.9±1.5,야교임고정조(6.3±2.9)겁명현강저,(P<0.01)。결론임고정환자VEGF표체장애발생재단백질번역화표체수평;VEGF적이상표체재임고정태반결양중구유중요적작용。
Objective To investigate relationship between the vascular endothelial growth factor (VEGF) and the pathogenesis of pregnancy induced hypertension syndrome (PIHs). Methods Twenty-three women with PIHs and twenty normal pregnant women were studied. The levels of VEGF in maternal and umbilical venous serum, placenta and decidual tissue from normal pregnancy and PIHs women were detected by enzyme linked immunosorbent assay (ELISA) and immunohistochemisty. Furthermore, the expression of VEGF mRNA in placenta and decidua was examined by reverse transcriptase polymerase chain reaction (RT-PCR). Results (1) The levels of VEGF in maternal blood were significantly lower in PIHs women than that in normal pregnancies wonen (10.4±3.8) ng/L and (17.0±9.3) ng/L (P<0.01). (2) The average gray of VEGF was determined on sections of placenta and decidua from PIHs or pregnancies women by computer image analysis. The expression of VEGF in placenta and decidua (69.0±8.9) and (55.0±7.3) was decreased significantly in PIHs women than that in normal pregnancies wonen (75.0±9.0) and (60.5±6.4, P<0.05). (3) The transcription levels of the VEGF mRNA in placenta and decidua were increased significantly in PIHs women than those in normal pregnancies women (4.6±3.2 vs 2.8±1.0;6.3±2.9 vs 3.9±1.5,P<0.01). Conclusions These findings suggested that the abnormal expression of VEGF in PIHs occured within the low-stream of genic transcription. It was considered that the abnormal expression of VEGF may play an important role in the pathogenesis of plcental ischemia in PIHs.