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正常妊娠及子癲前症孕婦胎盤組織中滋養層細胞其凋亡與增殖表現的研究
Apoptosis and Proliferation index in the Placental Trophoblasts Between Normal and Preeclampsia Women Compared
摘要
前言：子癲前症(preeclampsia)是一種在妊娠20週以後發生高血壓、蛋白尿及水腫的疾病，它的確實病理機轉目前未明，而胎盤就是一個重要因素。胎盤中的滋養層細胞(trophoblastic cell)凋亡(apoptosis)與增殖與子癲前症是否有關，目前研究的資料仍不多，本篇研究主要目的在比較子癲前症與正常懷孕胎盤，其滋養層細胞凋亡及增殖的表現是否有所不同，以期更了解及解釋子癲前症的病理機轉。 研究材料與方法：胎盤組織是從7位正常足月妊娠與7位子癲前症個案取出，她們皆是接受剖腹生產，細胞凋亡的研究是利用TUNEL（TdT-mediated dUTP-biotin nick end labeling，脫氧核糖核啟酸末端轉移媒瓷介導的缺口末端標記法）方法，在評估細胞增殖的方法是利用免疫組織化學染色法，測出Ki-67、Bcl-2，在滋養層細胞的免疫組織化學表現。結果評估方式則是利用下列兩項：一為positive index rate(%)代表染色有陽性反應者占所有細胞的比例。二為semiquantitative immunohistochemical Remmele score(IRS)。皆利用光學顯微鏡來做為計數工具，獲得平均值±標準差。比較子癲前症與正常者胎盤滋養層細胞在凋亡與增殖表現的不同。 研究結果：在子癲前症胎盤滋養層細胞發生細胞凋亡的平均值是0.37±0.04%，高於正常胎盤是0.18±0.05%。Ki-67的表現在子癲前症滋養層細胞發生的平均值是4.60±0.20%，高於正常胎盤3.96±0.39%；細胞凋亡與Ki-67的表現在子癲前症病人較正常者來的顯著明顯。而Bcl-2的IRS在子癲前症與正常者分別是3.70±0.86和4.03±1.25，子癲前症雖較正常者低，但統計學上無明顯意義。 結論：子癲前症胎盤的滋養層細胞Apoptosis及Ki-67的表現皆比正常者明顯增加，其原因可能和anti-apoptoticfactor(Bcl-2protein)表現減少，或是因為胎盤絨毛血管內膜細胞功能異常造成組織缺氧。可見這些因子的表現在子癲前症的病理機轉上扮演著一定角色。
並列摘要
Background and purpose: Preeclampsia is characterized by hypertension, edema, and proteinuria and its etiology remains unknown. Trophoblastic cell play an important role in the maintenance of placental function. However, information regarding to the roles of apoptosis and proliferation in the trophoblast of placenta in relation to the pathophysiology of preeclampsia. The aim of the study was to compare the difference between preeclampsia has been scanty and normal term pregnancy placenta in the expression of some proliferation and apoptotic/anti-apoptotic markers in the human placenta. Materials and Methods: Placental samples were obtained form 7 normal uncomplicated term pregnancy and 7 preeclampsia patients. Placenta samples were collected during cesarean section. Apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling(TUNEL) method. Expression of Ki-67, Bcl-2, were assessed using immunohistochemistry. The positive index rate (%) was defined as (positive stain cells/ total nuclei) X 100 and expressed as mean ± SD. The Bcl-2 was assessd by semiquantitative Immunohistochemical Remmele Score(IRS). For each placenta, 5 randomized fields are examined by light microscopy at a magnification of x 200(x 20 objective lens and x 10 eyepiece). Statistical significance was determined by using analysis of variance to compare the rates between normal and preeclampsia placentas. Statistical analysis was performed with the use of Mann Whitney U test. A p value of ＜0.05 was judged as significant. Result: The TUNEL-positive cells of the placenta were trophoblast with cluster of nuclei and the TUNEL-positive index of these cells was 0.37% ± 0.04% and normal placenta was 0.18% ± 0.05%. The Ki-67-positive index cells was 4.6% ± 0.2% and normal placenta was 3.9% ± 0.3%. The incidence of apoptosis and Ki-67 expression were significantly higher in preeclampsia placentas when compared with normal controls. Conversely Bcl-2 expression was lower generally in preeclampsia than normal, albeit no significant difference between the two groups was observed. Conclusion: These results suggest that trophoblast proliferation and apoptosis index may play a role in the pathophysiologic mechanisms of preeclampsia.