中华妇产科杂志
中華婦產科雜誌
중화부산과잡지
CHINESE JOUNAL OF OBSTETRICS AND GYNECOLOGY
2010年
10期
767-771
,共5页
宋学茹%张慧英%张艳芳%韩玉崑%李可君
宋學茹%張慧英%張豔芳%韓玉崑%李可君
송학여%장혜영%장염방%한옥곤%리가군
多囊卵巢综合征%丝裂原激活蛋白激酶类%细胞外信号调节MAP激酶类%子宫内膜增生%胰岛素抗药性%高胰岛素血症
多囊卵巢綜閤徵%絲裂原激活蛋白激酶類%細胞外信號調節MAP激酶類%子宮內膜增生%胰島素抗藥性%高胰島素血癥
다낭란소종합정%사렬원격활단백격매류%세포외신호조절MAP격매류%자궁내막증생%이도소항약성%고이도소혈증
Polycystic ovary syndrome%Mitogen-activated protein kinases%Extracellular signalregulated MAP kinases%Endometrial hyperplasia%Insulin resistance%Hyperinsulinism
目的 通过测定子宫内膜中胰岛素的丝裂原活化蛋白激酶(MAPK)/细胞外信号调节激酶(ERK)信号通路中ERK1/2(表示ERK1和ERK2,下同)的表达及其活化程度,探讨其在多囊卵巢综合征(PCOS)子宫内膜增生及癌变形成中的作用及意义,以及影响其表达及活化程度的因素.方法 选择2007年1月-2008年6月天津医科大学总医院行诊断性刮宫的PCOS患者52例(PCOS组),相匹配的非PCOS患者(良性卵巢肿瘤)32例为对照组.测定所有观察对象的空腹血糖及胰岛素水平;所有观察对象均行子宫内膜病理检查,按子宫内膜病理结果将PCOS组患者分为子宫内膜增生及癌变组(19例)和正常子宫内膜组(33例);根据是否存在胰岛素抵抗将PCOS组患者分为胰岛素抵抗组(38例)和非胰岛素抵抗组(14例).蛋白印迹法(western blot)检测子宫内膜中ERK1/2及其活化形式--磷酸化ERK1/2(p-ERK1/2)蛋白的表达水平.结果 (1)PCOS组患者子宫内膜中p-ERK1/2蛋白的表达水平[(61±13)%]高于对照组[(44±10)%],两组比较,差异有统计学意义(P＜0.01).(2)子宫内膜增生及癌变组子宫内膜中p-ERK1/2蛋白的表达水平[(70±11)%]高于正常子宫内膜组[(55±10)%],两组比较,差异有统计学意义(P＜0.01);胰岛素抵抗组子宫内膜中p-ERK1/2蛋白的表达水平[(63±13)%]高于非胰岛素抵抗组[(55±7)%],两组比较,差异有统计学意义(P＜0.01).(3)空腹胰岛素水平、胰岛素曲线下面积、体质指数与PCOS组患者子宫内膜中p-ERK蛋白的表达水平相关,相关系数分别为0.447、0.456、0.381(P均＜0.01).结论 PCOS患者子宫内膜存在MAPK/ERK信号通路的过度活化,与子宫内膜增生及癌变的发生有关;胰岛素抵抗及高胰岛素血症有促进ERK活化的作用.
目的 通過測定子宮內膜中胰島素的絲裂原活化蛋白激酶(MAPK)/細胞外信號調節激酶(ERK)信號通路中ERK1/2(錶示ERK1和ERK2,下同)的錶達及其活化程度,探討其在多囊卵巢綜閤徵(PCOS)子宮內膜增生及癌變形成中的作用及意義,以及影響其錶達及活化程度的因素.方法 選擇2007年1月-2008年6月天津醫科大學總醫院行診斷性颳宮的PCOS患者52例(PCOS組),相匹配的非PCOS患者(良性卵巢腫瘤)32例為對照組.測定所有觀察對象的空腹血糖及胰島素水平;所有觀察對象均行子宮內膜病理檢查,按子宮內膜病理結果將PCOS組患者分為子宮內膜增生及癌變組(19例)和正常子宮內膜組(33例);根據是否存在胰島素牴抗將PCOS組患者分為胰島素牴抗組(38例)和非胰島素牴抗組(14例).蛋白印跡法(western blot)檢測子宮內膜中ERK1/2及其活化形式--燐痠化ERK1/2(p-ERK1/2)蛋白的錶達水平.結果 (1)PCOS組患者子宮內膜中p-ERK1/2蛋白的錶達水平[(61±13)%]高于對照組[(44±10)%],兩組比較,差異有統計學意義(P＜0.01).(2)子宮內膜增生及癌變組子宮內膜中p-ERK1/2蛋白的錶達水平[(70±11)%]高于正常子宮內膜組[(55±10)%],兩組比較,差異有統計學意義(P＜0.01);胰島素牴抗組子宮內膜中p-ERK1/2蛋白的錶達水平[(63±13)%]高于非胰島素牴抗組[(55±7)%],兩組比較,差異有統計學意義(P＜0.01).(3)空腹胰島素水平、胰島素麯線下麵積、體質指數與PCOS組患者子宮內膜中p-ERK蛋白的錶達水平相關,相關繫數分彆為0.447、0.456、0.381(P均＜0.01).結論 PCOS患者子宮內膜存在MAPK/ERK信號通路的過度活化,與子宮內膜增生及癌變的髮生有關;胰島素牴抗及高胰島素血癥有促進ERK活化的作用.
목적 통과측정자궁내막중이도소적사렬원활화단백격매(MAPK)/세포외신호조절격매(ERK)신호통로중ERK1/2(표시ERK1화ERK2,하동)적표체급기활화정도,탐토기재다낭란소종합정(PCOS)자궁내막증생급암변형성중적작용급의의,이급영향기표체급활화정도적인소.방법 선택2007년1월-2008년6월천진의과대학총의원행진단성괄궁적PCOS환자52례(PCOS조),상필배적비PCOS환자(량성란소종류)32례위대조조.측정소유관찰대상적공복혈당급이도소수평;소유관찰대상균행자궁내막병리검사,안자궁내막병리결과장PCOS조환자분위자궁내막증생급암변조(19례)화정상자궁내막조(33례);근거시부존재이도소저항장PCOS조환자분위이도소저항조(38례)화비이도소저항조(14례).단백인적법(western blot)검측자궁내막중ERK1/2급기활화형식--린산화ERK1/2(p-ERK1/2)단백적표체수평.결과 (1)PCOS조환자자궁내막중p-ERK1/2단백적표체수평[(61±13)%]고우대조조[(44±10)%],량조비교,차이유통계학의의(P＜0.01).(2)자궁내막증생급암변조자궁내막중p-ERK1/2단백적표체수평[(70±11)%]고우정상자궁내막조[(55±10)%],량조비교,차이유통계학의의(P＜0.01);이도소저항조자궁내막중p-ERK1/2단백적표체수평[(63±13)%]고우비이도소저항조[(55±7)%],량조비교,차이유통계학의의(P＜0.01).(3)공복이도소수평、이도소곡선하면적、체질지수여PCOS조환자자궁내막중p-ERK단백적표체수평상관,상관계수분별위0.447、0.456、0.381(P균＜0.01).결론 PCOS환자자궁내막존재MAPK/ERK신호통로적과도활화,여자궁내막증생급암변적발생유관;이도소저항급고이도소혈증유촉진ERK활화적작용.
Objective To investigate the activation of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated protein kinase (ERK) signaling pathway in the endometrium of women with polycystic ovary syndrome (PCOS) and its effect and significance in the cause of hyperplasia and carcinoma;and investigate the factors which affect the activation of the MAPK/ERK signaling pathway. Methods Collected 52 patients diagnosed as PCOS who were taken dilation and curettage of uterus as study, while 32 non-PCOS patients matched as control group. Serum hormonal parameters, fasting blood glucose and insulin were measured in all patients. The PCOS patients were sub-group as insulin resistance group and non-insulin resistance group; all the patients were carried out pathology inspection of endometria, and the PCOS patients were sub-group as endometrial hyperplasia and carcinoma group and normal endometrium group based on the outcome of pathology inspection. Western blot were performed to detect the expressions of ERK1/2 and phosphorylated ERK1/2 (p-ERK1/2), the activation of ERK1/2. Results (1)The expression of pERK1/2 [(61 ±13)%] in the endometrium in PCOS group was higher than that in the control [(44 ±10)%, P ＜0.01]. (2)The expression of p-ERK1/2 was significantly increased in group of endometrial hyperplasia and carcinoma [ ( 70 ± 11 )% ] compared to that in group of normal endometrium [ (55 ± 10)% ,P ＜ 0.01 ], while there were significant difference between group of insulin resistance [ (63 ± 13 )% ] and group of non-insulin resistance [ (55 ±7)%, P ＜0.01 ]. (3) Fasting insulin level, insulin area under the curve and body mass index were related to the expression of p-ERK1/2 in endometrium with PCOS, the correlation coefficient were 0.447, 0.456 and 0.381, respectively ( all P ＜ 0.01 ). Conclusions The MAPK/ERK signaling pathway in endometrium with PCOS was overactivation, which was related to the endometrial hyperplasia and carcinoma; while the activation of MAPK/ERK signaling pathway were effected by insulin resistance and hyperinsulinemia.
