子宫内膜异位症患者血清中TNF-α、IL-8和SICAM-1水平测定的意义
|
摘要
研究背景：
子宫内膜内异症是一种严重影响育龄期妇女健康和生活质量的妇科多发病和常见病。其确切发病机制至今尚未完全阐明,在众多病因学说中,Sampson提出的经血逆流种植学说虽被多数学者接受,但此学说不能解释子宫内膜异位在盆腔外,也无法解释虽然多数(70%-90%)女性存在经血逆流现象,但只有少数(10%-15%)的妇女发病,说明它很有可能只是该病发病的诱因。近年来,随着分子生物学及免疫学技术的发展,越来越多的证据证明免疫调节异常在EM的发生、发展各环节起着至关重要的作用的,甚至很可能是决定性作用。
肿瘤坏死因子α(TNF-α):可诱导腹膜细胞表达一系列黏附分子,从而使腹膜细胞与子宫内膜细胞黏附作用增强,这是异位子宫内膜成功种植腹腔的第一步。
白细胞介素一8(IL-8):IL-8与其受体结合后可改变杀伤性T淋巴细胞表面表达Fas／Fas l系统,促进细胞毒性T淋巴细胞CTL(CTL)细胞的凋亡增加,腹腔内NK细胞活性下降,从而有助于异位内膜在腹腔种植时可以逃避机体的免疫监视。
可溶性细胞间粘附分子1(SICAM-1):SICAM-1的升高可以有效地阻断细胞毒性T淋巴(CTL)与靶细胞(子宫内膜细胞)结合,极大地降低了其对靶细胞的粘附、杀伤功能,也可使NK细胞活性受到封闭或削弱,减弱了NK细胞在免疫监视过程中所起的主要作用。
目的
拟通过酶联免疫吸附法检测子宫内膜异位症患者与正常非子宫内膜异位症者血清中IL-8.TNF-α及SICAM-1表达,研究三者的相关性,以探讨三者在子宫内膜异位症发病机制中的作用及在子宫内膜异位症临床诊断中的价值。
材料与方法
1.研究对象选取2010年7月至2011年7月在郑州大学第二附属医院妇科住院手术病人共69例,分子宫内膜异位症组和正常对照组,36例子宫内膜异位症患者(其中Ⅰ-Ⅱ期20例,Ⅲ一Ⅳ期16例)、33例对照组妇女。
研究对象筛选标准：内异症组和对照组患者均无内分泌、免疫和代谢性等相关性疾病,平素月经均较规律,术前3个月内未用过任何激素治疗。
2.研究方法：采用酶联免疫法(Elisa)测定内异症患者和对照组血清中TNF-α, IL-8, SICAM-1水平。实验结果处理运用SPSS17.0统计软件系统分析,以<0.05为差异有统计学意义。
结果
1.EM组血清TNF-α, IL-8, SICAM-1水平均高于对照组,差异有显著性(P<0.05),且EM组Ⅲ～Ⅳ期血清TNF-α,IL-8,SICAM-1水平高于Ⅰ～Ⅱ期,差异有显著性意义(P<0.05)。
2.内异症患者血清中IL-8, SICAM-1水平均与TNF-a水平呈线性正相关,IL-8与SICAM-1水平无线性关系。
3. TNF-a. IL-8和SICAM-1三种因子诊断内异症的特异性分别为48.48%、45.45%、60.61%；敏感性分别为44.44%、47.22%、69.44%。
结论
1. TNF-a, IL-8和SICAM-1均参与了EM的发病过程,且三者具有协同作
2.血清中SICAM-1在诊断内异症时有较高的敏感性和特异性,可望成为临床诊断内异症的指标。
Background and Purpose
Endometriosis (EM) is a multiple and common gynecologic disease which can seriously effect the health of women. The mechanism of EM has not been completely understood. It is well known that the hypothesis of endometrium exfoliative fragments transplantation which Sampson put forward has been accepted by most scholars. But this theory can't explain endometriosis outside the pelvic.It also can't explain most (70%-90%)women have menses blood backward phenomenon but only a few (10%-15%) of the women have suffered from it.With the development of the molecular biology and immunology technology,more more evidence shows that immune adjustment abnormalities may play a very important role in EM.
Tumor necrosis factor alpha (TNF alpha) can induce skin cells express a series of peritoneal adhesion molecules, which can cause adhesion enhancement between the peritoneum cells and endometrial cells. This is the first step of endometriosis to plant in the abdominal cavity.
Interleukin-8(IL-8) and its receptor may change the destruction of T lymphocyte surface expression Fas/Fas L system, promote an increase in the apoptosis of cell toxicity T lymphocytes CTL (CTL) cell, and intro-abdominal NK cell activity decline, which helps entopic endometrial plant in celiac escaping the immune monitoring.
The increasing of Soluble adhesion molecules between cells-1(SICAM-1) can decrease cell toxicity T (CTL) and lymphatic target cells (endometrial cells) union which lead the adhesion and killer function of its target cells, and make the NK cell activity closed or weakened. It can weaken the leading function of NK cells in the immune monitoring process.
In the present study, we detect the expression of IL-the8, TNF alpha and SICAM-1between endometriosis patients and normal, study the correlation of the three, investigate the mechanism of the three in endometriosis and the treatment of endometriosis.
Materials and method
1. We collected69samples of patients from July2010to July2011in the gynecology of the second affiliated hospital of Zhengzhou university.36patients with EM (20women with stage Ⅰ-Ⅱ,16women with stage III-IV),33cases of control group women (for other benign disease by laparoscopic surgery, or confirmed by operation or pelvic examination).
The selection standard of research object:EM group and control group were had no endocrine, immune or metabolic disease, who had a regular menstruation were preoperative3months and not used any hormone therapy.
2. The serum levels of TNF-α、IL-8and SICAM-1in endometritis patients and control patients were determined by ELISA. The results processing used SPSS17.0statistical software system to analyze, with P<0.05for differences with a statistical significance.
The results
1. The serum levels of TNF alpha, IL-8, SICAM-1in EM were higher than those in control group(P<0.05). The serum levels of TNF alpha, IL-8, SICAM-1in stage III-IV of EM were higher than that in stage I-II(P<0.05).
2. The serum level of IL-8, SICAM-1and TNF alpha level were linear related, IL-8and SICAM-1level were not linear related.
3. The specificity of TNF alpha, IL-8and SICAM-1were48.48%、45.45%and60.61%; and the sensitivity of the three were44.44%、47.22%and69.44%.
Conclusion
1. TNF alpha, IL-8and SICAM-1were involved in the pathogenesis of EM, and the three was synergistic.
2. Serum SICAM-1had higher sensitivity and specificity, so it was expected to become a clinical diagnosis of EM.
子宫内膜内异症是一种严重影响育龄期妇女健康和生活质量的妇科多发病和常见病。其确切发病机制至今尚未完全阐明,在众多病因学说中,Sampson提出的经血逆流种植学说虽被多数学者接受,但此学说不能解释子宫内膜异位在盆腔外,也无法解释虽然多数(70%-90%)女性存在经血逆流现象,但只有少数(10%-15%)的妇女发病,说明它很有可能只是该病发病的诱因。近年来,随着分子生物学及免疫学技术的发展,越来越多的证据证明免疫调节异常在EM的发生、发展各环节起着至关重要的作用的,甚至很可能是决定性作用。
肿瘤坏死因子α(TNF-α):可诱导腹膜细胞表达一系列黏附分子,从而使腹膜细胞与子宫内膜细胞黏附作用增强,这是异位子宫内膜成功种植腹腔的第一步。
白细胞介素一8(IL-8):IL-8与其受体结合后可改变杀伤性T淋巴细胞表面表达Fas／Fas l系统,促进细胞毒性T淋巴细胞CTL(CTL)细胞的凋亡增加,腹腔内NK细胞活性下降,从而有助于异位内膜在腹腔种植时可以逃避机体的免疫监视。
可溶性细胞间粘附分子1(SICAM-1):SICAM-1的升高可以有效地阻断细胞毒性T淋巴(CTL)与靶细胞(子宫内膜细胞)结合,极大地降低了其对靶细胞的粘附、杀伤功能,也可使NK细胞活性受到封闭或削弱,减弱了NK细胞在免疫监视过程中所起的主要作用。
目的
拟通过酶联免疫吸附法检测子宫内膜异位症患者与正常非子宫内膜异位症者血清中IL-8.TNF-α及SICAM-1表达,研究三者的相关性,以探讨三者在子宫内膜异位症发病机制中的作用及在子宫内膜异位症临床诊断中的价值。
材料与方法
1.研究对象选取2010年7月至2011年7月在郑州大学第二附属医院妇科住院手术病人共69例,分子宫内膜异位症组和正常对照组,36例子宫内膜异位症患者(其中Ⅰ-Ⅱ期20例,Ⅲ一Ⅳ期16例)、33例对照组妇女。
研究对象筛选标准：内异症组和对照组患者均无内分泌、免疫和代谢性等相关性疾病,平素月经均较规律,术前3个月内未用过任何激素治疗。
2.研究方法：采用酶联免疫法(Elisa)测定内异症患者和对照组血清中TNF-α, IL-8, SICAM-1水平。实验结果处理运用SPSS17.0统计软件系统分析,以<0.05为差异有统计学意义。
结果
1.EM组血清TNF-α, IL-8, SICAM-1水平均高于对照组,差异有显著性(P<0.05),且EM组Ⅲ～Ⅳ期血清TNF-α,IL-8,SICAM-1水平高于Ⅰ～Ⅱ期,差异有显著性意义(P<0.05)。
2.内异症患者血清中IL-8, SICAM-1水平均与TNF-a水平呈线性正相关,IL-8与SICAM-1水平无线性关系。
3. TNF-a. IL-8和SICAM-1三种因子诊断内异症的特异性分别为48.48%、45.45%、60.61%；敏感性分别为44.44%、47.22%、69.44%。
结论
1. TNF-a, IL-8和SICAM-1均参与了EM的发病过程,且三者具有协同作
2.血清中SICAM-1在诊断内异症时有较高的敏感性和特异性,可望成为临床诊断内异症的指标。
Background and Purpose
Endometriosis (EM) is a multiple and common gynecologic disease which can seriously effect the health of women. The mechanism of EM has not been completely understood. It is well known that the hypothesis of endometrium exfoliative fragments transplantation which Sampson put forward has been accepted by most scholars. But this theory can't explain endometriosis outside the pelvic.It also can't explain most (70%-90%)women have menses blood backward phenomenon but only a few (10%-15%) of the women have suffered from it.With the development of the molecular biology and immunology technology,more more evidence shows that immune adjustment abnormalities may play a very important role in EM.
Tumor necrosis factor alpha (TNF alpha) can induce skin cells express a series of peritoneal adhesion molecules, which can cause adhesion enhancement between the peritoneum cells and endometrial cells. This is the first step of endometriosis to plant in the abdominal cavity.
Interleukin-8(IL-8) and its receptor may change the destruction of T lymphocyte surface expression Fas/Fas L system, promote an increase in the apoptosis of cell toxicity T lymphocytes CTL (CTL) cell, and intro-abdominal NK cell activity decline, which helps entopic endometrial plant in celiac escaping the immune monitoring.
The increasing of Soluble adhesion molecules between cells-1(SICAM-1) can decrease cell toxicity T (CTL) and lymphatic target cells (endometrial cells) union which lead the adhesion and killer function of its target cells, and make the NK cell activity closed or weakened. It can weaken the leading function of NK cells in the immune monitoring process.
In the present study, we detect the expression of IL-the8, TNF alpha and SICAM-1between endometriosis patients and normal, study the correlation of the three, investigate the mechanism of the three in endometriosis and the treatment of endometriosis.
Materials and method
1. We collected69samples of patients from July2010to July2011in the gynecology of the second affiliated hospital of Zhengzhou university.36patients with EM (20women with stage Ⅰ-Ⅱ,16women with stage III-IV),33cases of control group women (for other benign disease by laparoscopic surgery, or confirmed by operation or pelvic examination).
The selection standard of research object:EM group and control group were had no endocrine, immune or metabolic disease, who had a regular menstruation were preoperative3months and not used any hormone therapy.
2. The serum levels of TNF-α、IL-8and SICAM-1in endometritis patients and control patients were determined by ELISA. The results processing used SPSS17.0statistical software system to analyze, with P<0.05for differences with a statistical significance.
The results
1. The serum levels of TNF alpha, IL-8, SICAM-1in EM were higher than those in control group(P<0.05). The serum levels of TNF alpha, IL-8, SICAM-1in stage III-IV of EM were higher than that in stage I-II(P<0.05).
2. The serum level of IL-8, SICAM-1and TNF alpha level were linear related, IL-8and SICAM-1level were not linear related.
3. The specificity of TNF alpha, IL-8and SICAM-1were48.48%、45.45%and60.61%; and the sensitivity of the three were44.44%、47.22%and69.44%.
Conclusion
1. TNF alpha, IL-8and SICAM-1were involved in the pathogenesis of EM, and the three was synergistic.
2. Serum SICAM-1had higher sensitivity and specificity, so it was expected to become a clinical diagnosis of EM.
引文
[1]乐杰.妇产科学[M].第七版.北京：人民卫生出版社,2007：326.
[2]McLain J, Dealt G,Prentice A, et al. Decreased levels of the potent regular of monocyte/macrophage activation, interleukin-13, in the peritoneal fluid of patients with endometriosis. Hum Re prod,1997;12:1307-1310.
[3]America Fertility Society. Revised America fertility society classification of endometriosis:1985. Fer til Steil,1985;43:351-354.
[4]Hamada T, Higashiosaka H, Hyoidal S, et al. Peritoneal fluid concentrations of the cytokine RANTES correlate with the severity of endometriosis. Am J Obe tet Gyne col, 1993;9:1545-1549.
[5]Puniness J, Isolate K, Rasta H, et al. Increased levels of interleukin-6 and interleukin-10 in peritoneal fluid of patients with endometriosis. Am J Obstet Gyne cal,1996; 174(5): 1522-1526.
[6]Ryan IP, Ts eng JF, Schrik ED, et al. Interleukin-8 concentrations are elevated in peritoneal fluid of women with endometriosis. Fer til Sterile,1995;63:929-932.
[7]Amici A, Takeout SL, Hart E, et al. Interleukin-8 concentration in peritoneal fluid of patients with endometriosis and modulation of interleukin-8 expression human mesothelial cells. Mol Hun Re prod,1996;2(1):40-45.
[8]Korma N, Matsuyama K, Oka mura H. Cytokines in the peritoneal fluid of patients with endometriosis. Int J Gyne col Obstet,1993;43(1):45-50.
[9]Rana N, Braun DP, House R, et al. Basal and stimulated secretion of cytokines by peritoneal macrophage in women with endometriosis. Fer til Steil,1996;65:925-930.
[10]Riel SE, Groupisms PN, Hus X, et al. Overregulation of interleukin-6 responses in ectopic endometrial stromal cells:correlation with decreased soluble receptor levels in peritoneal fluid of women with endometriosis. J Clint Endocrinal Me tab,1995;80:1473-1477.
[11]Hamada T, Enate A, Lunarist M, et al. Role of cytokine in progression of endometriosis. Gyne col Obstet Invest,1997,47suppll:34-40.
[12]Vader Linden PJ.Theories on the pathogenesis of endometriosis.Hum Re prod,1996, 11:53-65.
[13]Lunisolar M,Asanas-Roux F, Donne J.Early stage endometriosis:adhesion and growth of human menstrual endometrium in nude mice. Fer til Steil,2000,74:306-312.
[14]Primula N,Saluda A,Epiloguize-Kalispel O, et al.Regulation of endometrial stromal cell matrix metropolitanate activity and invasiveness by interleaf-8. Fer til Steil,2004,81:904-911.
[15]Galvani R,Smith L,Fowler PA.Effect of interleukin-8,anti-IL-8, and IL-12on endometrial cell survival in combined endometrial gland and stromal cell cultures derived from women with and without endometriosis. Fer til Steil,2002.Jan;77(1):62-70.
[16]Aba Y, Hamada T, Horae S, et al. Lipopolysaccharide-promoted prefiguration of endometriosis stromal cells via induction of tumor necrosis factor alpha and interleukin-8 expression[J].Fer til Steil,2004,82[suppl3]:1036-1042.
[17]Biwabik T, Hamada T, Terai N, Role of autokinesis in endometriosis associated infertility[J]. Gyne col Obstet Invest,2002,53(Supp 11):11.
[18]Braun DP, Ding J, Stokowski WP. Peritoneal fluid-mediated enhancement of ectopic and ectopic endometrial cell proliferation is dependent on tumor necrosis factor-alpha in women with endometriosis[J]. Fer til Steel,2002,78(4):727-732.
[19]Riel S, Foster WG. Environmental dioxin and endometriosis[J]. Toxical Sci,2002,70(2): 161-170.
[20]Toyama N, Matsuyama K, Oka mura H. Cytokines in the peritoneal fluid of patient as with endometriosis. Int J Gyne col Obstet,1993;43(1):45-50.
[21]周家德.血清和腹腔液中自介素6、8及肿瘤坏死死因子a与子宫内膜异位症病因相关性的研究[D].安徽：安徽医科大学硕十论文,2002.
[22]黄鲁.子宫内膜异位症患者血清及腹腔液中IL-6、TNF-a水平的测定及临床意义[D].宁夏：宁夏医科大学硕士论文,2009.
[231徐红.细胞因子IL-6、IL-8及TNF-a在子宫内膜异位症发生发展中的意义[D].广西：广西医科大学硕士论文,2007.
[24]Melia M, Pace E, Siena L, Raspatory M, Lipa A, Prof ita M, Bon anno A, Vignola AM, Bon signore G, Moody CH, Monomark M. Biologically active intercellular adhesion molecule-1 is shed as dimmers by a regulated mechanism in the inflamed pleural space. Am J Perspire Crit Care Med.2003 Apr 15;167(8):1131-1138.
[25]Hahn JJ, Chow JW, Home GJ, Maj BK, Ene reman JT, Hoffman P, Hugh JC. MUC1 mediates trans endothelial migration in visto by ligating endothelial cell ICAM-1. Cain Exp Metastasis.2005;22(6):475-483.
[26]伍俊萍,张俊慧,刘银坤等.腹腔液中sic am-1、TNF-a水平与子宫内膜异位症.中国优生与遗传杂志,2005,13；66-67..
[27]Somalian E, Viga no P, Garifuna B, Guarneri D, Maccabeus M, Vigneron M. Human endometrial cells as a source of soluble intercellular adhesion molecule-1. Hum Replay. 1996 Jun; 11 (6):1190-1194.
[28]Somalian E, Viga no P, Garifuna B, Guarneri D, Maccabeus M, Vigneron M. Human endometrial cells as a source of soluble intercellular adhesion molecule-1. Hum Replay. 1996 Jun; 11 (6):1190-1194.
[29]Korzybski P, Wozniak J, Op ala T. Production of soluble intracellular adhesion molecule-1(SICAM-1) in human endometrial cell culture. Wadi Lek.2003;56(9-10): 430-433.
[30]Rel ova AJ, Shah ana S, Makeyevka N, Romanos GM. Effect of cytokines on ICAM-1 and ZO-1 expression on human airway epithelial cells. Cell Biol Int.2005 esp;29(9):768-77.
[31]De Placedo, Somalian E, Di Blaster AM,Coolin o S, Candid M, Vigneron M. Suppression of natural killer cell function and production of soluble ICAM-1:endometrial stroma versus melanoma. Am J Re prod Immunologic.2001 nova;46(5):342-348.
[32]樊冬梅SICAM-1和CA125在子宫内膜异位症诊断中的的意义[D].河南：郑州大学硕士论文,2007.
[33]Kumamoto Y,Hamada T,Horae S,et al.Tumor necrosis factor-alpha-induced interleukin-8(IL-8) expression in endometrioses stromal cells,probably through nuclear factor kappa B activation:gonadotropin-releasing hormone ago-inst treatment reduced IL-8 expression.Cain Endocrinal Me tab,2003,88(2):730-735.
[34]Hoffnung D,K lingel K,Doorn K,et al.Regulated on activation,normal T-cell expressed and secreted m RNA expression in normal endometrium and endometrial implants: assessment of auto crine/Paracelsus in regulation by hypersensitization[J]. Pathol,2001, 158(6):1949-1954.
[35]Lee G H, Chi Y M, Kim S H,et al. Association of tumor necrosis factor-(alpha) gene polymorphisms with advanced stage endometriosis[J].Hum Re prod,2008,23(4):977-981.
[36]Viga no P, Somalian E, Di Blaster AM, et al. Suppression of natural killer cell function and production of soluble ICAM—1:endometrial stroma versus melanoma. Am J Re prod, 2001, Nov,46(5):342-348.
[37]Thomson AJ, Greer MR Young A, etal. Expression of intercellular adhesion molecules ICAM-1 and ICAM-2 in human endometrium:regulation by interferon-gamma. Mol Hum Re prod,1999,5(1):60-64.
[38]Somalian E,Viga no P,Candida M,Felicitator I,Di Blaster AM,Vigneron M.Use of serum-soluble intercellular adhesion molecule-1 as a new marker of endometriosis.Fer til Steel.2002 May;77(5):1028-1031.
[1]Danish M,Anus k,Fukuoka J,et al.Down-regulation of interleukin-I recept er type I expression of CXC chemokineses in endometrial stromal cells:a possible mechanism for the altered immunological functions in endometriosis[J].cline Endocrinal Me tab,资料2004, 89(10):5094-5100.
[2]Keenan JA,Chen TT,Cadwell NL,et al,IL-lbeta,TNF-alpha and IL-2 in peritoneal fluid and macrophage-conditioned media of women with endometriosis [J].Am J Re prod Immunologic,1995,34(6):381-385.
[3]Liveborn DI,Bent F,Chao VA,et al.Induction of an angiogenic phenotype in endometrioses stroma 11 cell cultures by interleukin-I beta [J].Mol Hum Record,2000,6(3):269-275.
[4]张淑芝,王慧芝,孟藏者：子宫内膜异位症并不孕患者腹腔淋巴细胞及其白细胞介素-2的变化[J]。中华妇产科杂志,1998,33：17-19.
[5]CHAOUAT G,MENU E,CLARK DA,et a 1.Control of fetal survival nival in CBA/2 mice by lymphokine therap[J].J Re prod Ferrol,1990,89:447-458.
[6]WEED JC,ARQUEMBOURG P C.Endometriosis:Call it produce all autoimmune response resulting in infertility?Cain Ob ster Gyne col,1980,23:885-893
[7]TARTAKOVSKY B,GOLD STEIN O,BROSH N.Colony-Stein-elating factor-1 blocks early pregnancy in mice[J].Biol Re prod,1991,44:906-912.
[8]Rana N.Braun DP,House R, et al.Basal and stimulated secretion of cytokines by peritoneal macrophages in women with endometriosis.Fer til Steil,1996;65:925-930.
[9]Ts udo T,Hamada T,lake T, et al.Altered gene expression and secretion of interleukin-6 in stromal cells droved from endometrial tissue[J].Fer til Steil,2000,73:1205-1211.
[10]Schroeder W,Garget R, Interleukin-6 receptor in peritoneal fluid and serum of patients with endometriosis [J].Cain Exp Obstet Gyne col,1996,23(1):10-14.
[11]朱剑飞,陈友国,杨伟文：子宫内膜异位症患者血清及腹腔液白介索-6的临床意义[J].江苏医药杂志,2004,5(30)：362-363.
[12]BERPUIST A,BRUSE C,CARLBERG M,et al.Interleukin I-beta,Interleukin-6 and tumor necrosis factor-alpha in endomorphic fid due and in endometrium[J].Fer til Steil,2001, 5:489-495.
[13]Bedawin MA,Falcon T, et al.Prediction of endometriosis with serum and peritoneal fluid markers:a prospective controlled trial [J].Hum Record,2002,Fed,17(2):426-431.
[14]Song M,Carabine SA,Taradiddle N,et al.Presence of endometrial epithelial cell in the peritoneal cavity and the mesothelial inflammatory response[J].Fer til Steil,2003,79(Suppl 1):789-794.
[15]Barca E,Rozzer ES,Kolinski E et al.Angiogenic activity and IL-8 concentrations in peritoneal fluid and sers in endometriosis [J] Intt Gynecologic Obstet,2002,79(3):229-235.
[16]Aubergiste A,Netty H,Saffrony B, et al.Production of interleukins 1 beta,6 and 8 and tumor necrosis factor alpha in separated and cultured endometrial and endometrial stromal and epithelial cells.Gyne col Obstet Invest,2000;50(1):1-6.
[17]Vader Linden PJ.Theories on the pathogenesis of endometriosis.Hum Re prod,1996, 11:53-65.
[18]Lunisolar M,Casabas-Roux F, Donne J.Early stage endometriosis:adhesion and growth of human menstrual endometrium in nude mice. Fer til Steil,2000,74:306-312.
[19]Primula N,Saluda A,Epiloguize-Kalispel O, et al.Regulation of endometrial stromal cell matrix metropolitanate activity and invasiveness by interleukin-8. Fer til Steil,2004, 81:904-911.
[20]Galvani R,Smith L,Fowler PA.Effect of interleukin-8,anti-IL-8, and IL-12on endometrial cell survival in combined endometrial gland and stromal cell cultures derived from women with and without endometriosis. Fer til Steil,2002.Jan;77(1):62-70.
[21]Bacchante R,Bugler M,Touraine JL, et al.High levels of interleukin-10 production in vivo are associated with tolerance in patients transplanted with HLA mismatched hematopoietic stem cells.J Exp Med,1994; 179:493-502.
[22]Puniness J,Isolate K,Rasta H,et al,Increased levels of interleukin-6 and interleukin-10 in peritoneal fluid of patients with endometriosis.Am J Obstet Gyne col,1996; 174(5): 1522-1526.
[23]Biwabik T, Hamada T,et al.Tumor necrosis factor-alpha Promotes proliferation of endometrial stromal cells by inducing interleukin-8 gene and protein expression[J].Cline Endocrinal Meta,2000,85(2):824-829.
[24]林俊,张信美,邓琳,等.子宫内膜异位症患者血清和腹腔液中自细胞介素-2,1,6的检测[J].浙江大学学报(医学版),2005,34(3)：161-163.
[25]Con ti P,Tempura D,Dander K,et al. Interleukin-16 network in inflammation and allergy[J].Allergy Asthma Proc,2002,23(2):103-108.
[26]Amici A,Mesotheliomata I.Glutenous A,et al.Increased level of interleukin-15 in the peritoneal fluid of women with endometriosis:inverse correlation with stage and depth of invasion[J].Hum Re prod,2003,18(2):429-432.
[27]Roku H,Tsuris Y,Krishnamurti SI,et al.Role of interleukin-18 in pathogenesis of endometriosis[J]. Hum Re prod,2004,19(3):709-714.
[28]Aria A,Mesotheliomata I,Noumenon, et al. Altered expression of interleukin-18 in the peritoneal fluid of women with endometriosis[J]. Fer til Steil,2003,80(4):889-894.
[29]Aba Y, Hamada T,Horae S, et al.Lipopolysaccharide-promoted proliferation of densitometric stromal cells via induction of tumor necrosis factor alpha and interleukin-8 expression[J]. Fer til Steil,2004,82[Suppl3]:1036-1042.
[30]Bergama A,Burse C,Carl berg M, et al. interleukin-6 and tumor necrosis factor in endometrium [J]. Fer til Steil,2001,75:489-495.
[31]Phillips DG,Stone AM,Jones BD, et al.Vascular permeability factor(rhVEGF165) stellulate direct angiogenesis in the rabbit cornea in vivo.At tiki,1994;8:961-965.
[32]Park JE,Keller GA,Ferrara N.The vascular endothelial growth factor (VEGF) microfonns:differential deposition into the sub epithelial extracellular matrix and bioactivity of extracellular matrix-bound VEGF.Mol Biol cell,1993;4:1317-1324.
[33]Mahoe JL;Dago d MY;Han g JC Vascular endothelial growth factor and interleukin-6 in peritoneal fluid of women with endometriosis [J].Fer til Steil,2000,73(11):166-170.
[34]Reckoning PR;Kennedy SH;Bark ow DH.Endometrial disease:the role of peritoneal fluid[J].Hum Re pod Undate,1998,4(5):741-757.
[35]Biwabik T;Hamada T;Ts udo T Tumor necrosis factor-alpha promotes proliferation of endometrial stromal cells by inducing interleukin-8 gene and protein expression [J].J Cain Endorse Me tab,2000,85(2):824-829.
[36]蔡松园,赵淑萍.止痛化胶囊对子宫内膜异位症患者血清CA125及VEGF的影响[J].山东医药,2009,49(21)：77--78.
[37]Clarence J,Prentice A,Char nock-Jones DC,et al.Vascular endothelial growth factor concentrations are elevated in peritoneal fluid of women with endometriosis[J].Hum Re pod,1996;11(1):220-223.
[38]Bota T, Fuji I, Wana H, et al. Reduced HGF expression in subcutaneous C T26 tumor genetically modified to secrete NK4 and its possible relation with antitumor effects[J]. Cancer Sci,2004,95(4):321-327.
[39]Khan KN, Mikasuki H, Fuji A. et al. Peritoneal fluid and serum levels of hepatocyte growth factor may predict the activity of endometriosis[J]. Acta obstet Gyne col Sand,2006,85(4): 458-466.
[40]宗利丽,汀龙霞,赵军,等。干细胞生长因子及其受体在子宫内膜异位症动物模型的表达[J]。广东医学,2008,29(10)：1646-1648.-
[41]宗利丽,李亚里,哈小琴.子宫内膜异位症患者腹水与血清中肝细胞生长因子的检测[J].第一军医大学学报,2003,23(8)：757-759.
[42]宗利丽,李亚里,宋三泰,等.子宫内膜异位症患者肝细胞生长因子及其受体c-Met的表达[J].第一军医大学学报,2004,24(6)：619-621.
[43]闫桂英,郑慕白,章汉旺等.细胞间粘附分子-1在子宫内膜异位症患者在位内膜、腹腔液及异位病灶中的表达及分析.实用J妇产科杂志,2005,21：158-160.
[44]潘莉莉,秦伶,卢丽萍等.腹腔液中SICAM-1、TNF-a水平与子宫内膜异位症.中国优生与遗传杂志,2005,13：66-67.
[45]伍俊萍,张俊慧,刘银坤等.整合素B和细胞粘附分子在子宫内膜异位症在位内膜与异位内膜组织中的的表达.中华妇产科杂志,1999,34-204-206.
[46]徐兰芝,李亚里.子宫内膜异位症新标志物SIC AM-1的临床研究[D].北京：中国人民解放军军事进修学院硕十学位论文,2006.
[47]樊冬梅SICAM-1和CA125在子宫内膜异位症诊断中的意义[D].河南：郑州大学硕士学位论文,2006.
[48]Doghole TM,Miao L,Hill JA.Cytokine profiles in autologous peritoneal fluid and peripheral blood of women with dee and superficial endometriosis[J].Arch Gyne col Obstet,2001,265(1):41-44.
[49]Syllogize K,Kinetochore H,Banksia M, et al.The involvement of T lymphocytes in the pathogenesis of endometrial tissues overgrowth in women with endometriosis[J].Mediators Inflame,2003,12(3):131-138.
[50]王志萍,蔡呈香.血清cA125检测在妇科病临床应用的评价[J].海峡医学,2005,17(1)：61-63.
[51]金帆.子宫内膜异位症患者血清和腹水CA125水平测定[J].国外医学：妇产科分册,1995,22(2)：126.
[52]戚瑞珍,李亚里,关峥.CA125在子宫内膜异位症中的临床意义[J].中国妇幼保健,2007,22(26)：36443645.
[53]Danes AM, Irani K, Goldschmidt Clermont PJ, et al. A requirement for carl in the PDGF-stimulated migration of fibroblasts and vascular smooth cells[J].Biochemical Mol Biolint,1998,45(2):279-287.
[54]Inone K, Cynthia O, Kawabata Y, et al. Effect of BO-653 and protocol on c-myc and PDGF A messenger RNA of the artery after balloon denudation in cholesterol-fed rabbits[J]. Atheroscleroses,2002,161(2):353-363.
[55]Latchkey MW. Schlitz A. Volar B, et al. Combined inhibition of vascular endothelial growth factor(VEGF), fibroblast growth factor and platelet derived growth factor, but not inhibition of VEGF alone, effectively suppresses an-Gio-genesis and vessel maturation in endometriosis lesions[J]. Hum Re prod,2006,21(1):262-268.
[56]Overton C. Fernandez Shaw S, Hicks B, el al. Peritoneal fluid cytokines and the relationship with endometriosis and pain[J]. Hum Re prod,1996,11(2):380-386.
[57]Tutelage M, Lauren J, Berg sten E, et al. Chromosomal location, ex on structure, and vascular expression patterns of the human PDGFC and PDGFD genes[J]. Circulation, 2001,103(18):2242-2247.
[58]闫华,许俊华,郭淑青等.子宫内膜异位症患者血清及腹腔液中血小板衍生生长因子,血.管细胞粘附分子水平的变化及其意义.[J].生殖医学杂志,2008,17(5)；342-345.
[59]Bhang L, Yang N. Tumor—derived Vascular En dot Belial Growth Favor Up—regulates erythropoietin blood vessels-2 in Host En Doth Ilium and Destabilizes Host Vasculature, Supporting Angiogenesis in Ovarian Cancer[J]. Cancer Research,2003,63(12): 3403-3412.
[60]Goren H, Animistic K, Ivan K, et al. FGF-1 and SIOOA 13 Possibly Contribute to Angiogenesis in all endometrioses[J]. J Re prod Immunology,2005,67(1/2):87-101.
[61]Saite M, Hamadryas M, Shibuichi M, et al. Induction of Tube Formation by Angiotensin Endothelial Cell/FI bioblast Coculture Is Dependent on Endogenous VEGF[J]. Cancer Science,2003,94:782-790.
[62]Gill KA, Brindle NP. Angiotensin-2 Stimulates M ignition of En-endothelia Progenitors and Their Interaction with Endothelium[J]. Bio chem Bio phys Res Commune,2005, 336(2):392-396.
[2]McLain J, Dealt G,Prentice A, et al. Decreased levels of the potent regular of monocyte/macrophage activation, interleukin-13, in the peritoneal fluid of patients with endometriosis. Hum Re prod,1997;12:1307-1310.
[3]America Fertility Society. Revised America fertility society classification of endometriosis:1985. Fer til Steil,1985;43:351-354.
[4]Hamada T, Higashiosaka H, Hyoidal S, et al. Peritoneal fluid concentrations of the cytokine RANTES correlate with the severity of endometriosis. Am J Obe tet Gyne col, 1993;9:1545-1549.
[5]Puniness J, Isolate K, Rasta H, et al. Increased levels of interleukin-6 and interleukin-10 in peritoneal fluid of patients with endometriosis. Am J Obstet Gyne cal,1996; 174(5): 1522-1526.
[6]Ryan IP, Ts eng JF, Schrik ED, et al. Interleukin-8 concentrations are elevated in peritoneal fluid of women with endometriosis. Fer til Sterile,1995;63:929-932.
[7]Amici A, Takeout SL, Hart E, et al. Interleukin-8 concentration in peritoneal fluid of patients with endometriosis and modulation of interleukin-8 expression human mesothelial cells. Mol Hun Re prod,1996;2(1):40-45.
[8]Korma N, Matsuyama K, Oka mura H. Cytokines in the peritoneal fluid of patients with endometriosis. Int J Gyne col Obstet,1993;43(1):45-50.
[9]Rana N, Braun DP, House R, et al. Basal and stimulated secretion of cytokines by peritoneal macrophage in women with endometriosis. Fer til Steil,1996;65:925-930.
[10]Riel SE, Groupisms PN, Hus X, et al. Overregulation of interleukin-6 responses in ectopic endometrial stromal cells:correlation with decreased soluble receptor levels in peritoneal fluid of women with endometriosis. J Clint Endocrinal Me tab,1995;80:1473-1477.
[11]Hamada T, Enate A, Lunarist M, et al. Role of cytokine in progression of endometriosis. Gyne col Obstet Invest,1997,47suppll:34-40.
[12]Vader Linden PJ.Theories on the pathogenesis of endometriosis.Hum Re prod,1996, 11:53-65.
[13]Lunisolar M,Asanas-Roux F, Donne J.Early stage endometriosis:adhesion and growth of human menstrual endometrium in nude mice. Fer til Steil,2000,74:306-312.
[14]Primula N,Saluda A,Epiloguize-Kalispel O, et al.Regulation of endometrial stromal cell matrix metropolitanate activity and invasiveness by interleaf-8. Fer til Steil,2004,81:904-911.
[15]Galvani R,Smith L,Fowler PA.Effect of interleukin-8,anti-IL-8, and IL-12on endometrial cell survival in combined endometrial gland and stromal cell cultures derived from women with and without endometriosis. Fer til Steil,2002.Jan;77(1):62-70.
[16]Aba Y, Hamada T, Horae S, et al. Lipopolysaccharide-promoted prefiguration of endometriosis stromal cells via induction of tumor necrosis factor alpha and interleukin-8 expression[J].Fer til Steil,2004,82[suppl3]:1036-1042.
[17]Biwabik T, Hamada T, Terai N, Role of autokinesis in endometriosis associated infertility[J]. Gyne col Obstet Invest,2002,53(Supp 11):11.
[18]Braun DP, Ding J, Stokowski WP. Peritoneal fluid-mediated enhancement of ectopic and ectopic endometrial cell proliferation is dependent on tumor necrosis factor-alpha in women with endometriosis[J]. Fer til Steel,2002,78(4):727-732.
[19]Riel S, Foster WG. Environmental dioxin and endometriosis[J]. Toxical Sci,2002,70(2): 161-170.
[20]Toyama N, Matsuyama K, Oka mura H. Cytokines in the peritoneal fluid of patient as with endometriosis. Int J Gyne col Obstet,1993;43(1):45-50.
[21]周家德.血清和腹腔液中自介素6、8及肿瘤坏死死因子a与子宫内膜异位症病因相关性的研究[D].安徽：安徽医科大学硕十论文,2002.
[22]黄鲁.子宫内膜异位症患者血清及腹腔液中IL-6、TNF-a水平的测定及临床意义[D].宁夏：宁夏医科大学硕士论文,2009.
[231徐红.细胞因子IL-6、IL-8及TNF-a在子宫内膜异位症发生发展中的意义[D].广西：广西医科大学硕士论文,2007.
[24]Melia M, Pace E, Siena L, Raspatory M, Lipa A, Prof ita M, Bon anno A, Vignola AM, Bon signore G, Moody CH, Monomark M. Biologically active intercellular adhesion molecule-1 is shed as dimmers by a regulated mechanism in the inflamed pleural space. Am J Perspire Crit Care Med.2003 Apr 15;167(8):1131-1138.
[25]Hahn JJ, Chow JW, Home GJ, Maj BK, Ene reman JT, Hoffman P, Hugh JC. MUC1 mediates trans endothelial migration in visto by ligating endothelial cell ICAM-1. Cain Exp Metastasis.2005;22(6):475-483.
[26]伍俊萍,张俊慧,刘银坤等.腹腔液中sic am-1、TNF-a水平与子宫内膜异位症.中国优生与遗传杂志,2005,13；66-67..
[27]Somalian E, Viga no P, Garifuna B, Guarneri D, Maccabeus M, Vigneron M. Human endometrial cells as a source of soluble intercellular adhesion molecule-1. Hum Replay. 1996 Jun; 11 (6):1190-1194.
[28]Somalian E, Viga no P, Garifuna B, Guarneri D, Maccabeus M, Vigneron M. Human endometrial cells as a source of soluble intercellular adhesion molecule-1. Hum Replay. 1996 Jun; 11 (6):1190-1194.
[29]Korzybski P, Wozniak J, Op ala T. Production of soluble intracellular adhesion molecule-1(SICAM-1) in human endometrial cell culture. Wadi Lek.2003;56(9-10): 430-433.
[30]Rel ova AJ, Shah ana S, Makeyevka N, Romanos GM. Effect of cytokines on ICAM-1 and ZO-1 expression on human airway epithelial cells. Cell Biol Int.2005 esp;29(9):768-77.
[31]De Placedo, Somalian E, Di Blaster AM,Coolin o S, Candid M, Vigneron M. Suppression of natural killer cell function and production of soluble ICAM-1:endometrial stroma versus melanoma. Am J Re prod Immunologic.2001 nova;46(5):342-348.
[32]樊冬梅SICAM-1和CA125在子宫内膜异位症诊断中的的意义[D].河南：郑州大学硕士论文,2007.
[33]Kumamoto Y,Hamada T,Horae S,et al.Tumor necrosis factor-alpha-induced interleukin-8(IL-8) expression in endometrioses stromal cells,probably through nuclear factor kappa B activation:gonadotropin-releasing hormone ago-inst treatment reduced IL-8 expression.Cain Endocrinal Me tab,2003,88(2):730-735.
[34]Hoffnung D,K lingel K,Doorn K,et al.Regulated on activation,normal T-cell expressed and secreted m RNA expression in normal endometrium and endometrial implants: assessment of auto crine/Paracelsus in regulation by hypersensitization[J]. Pathol,2001, 158(6):1949-1954.
[35]Lee G H, Chi Y M, Kim S H,et al. Association of tumor necrosis factor-(alpha) gene polymorphisms with advanced stage endometriosis[J].Hum Re prod,2008,23(4):977-981.
[36]Viga no P, Somalian E, Di Blaster AM, et al. Suppression of natural killer cell function and production of soluble ICAM—1:endometrial stroma versus melanoma. Am J Re prod, 2001, Nov,46(5):342-348.
[37]Thomson AJ, Greer MR Young A, etal. Expression of intercellular adhesion molecules ICAM-1 and ICAM-2 in human endometrium:regulation by interferon-gamma. Mol Hum Re prod,1999,5(1):60-64.
[38]Somalian E,Viga no P,Candida M,Felicitator I,Di Blaster AM,Vigneron M.Use of serum-soluble intercellular adhesion molecule-1 as a new marker of endometriosis.Fer til Steel.2002 May;77(5):1028-1031.
[1]Danish M,Anus k,Fukuoka J,et al.Down-regulation of interleukin-I recept er type I expression of CXC chemokineses in endometrial stromal cells:a possible mechanism for the altered immunological functions in endometriosis[J].cline Endocrinal Me tab,资料2004, 89(10):5094-5100.
[2]Keenan JA,Chen TT,Cadwell NL,et al,IL-lbeta,TNF-alpha and IL-2 in peritoneal fluid and macrophage-conditioned media of women with endometriosis [J].Am J Re prod Immunologic,1995,34(6):381-385.
[3]Liveborn DI,Bent F,Chao VA,et al.Induction of an angiogenic phenotype in endometrioses stroma 11 cell cultures by interleukin-I beta [J].Mol Hum Record,2000,6(3):269-275.
[4]张淑芝,王慧芝,孟藏者：子宫内膜异位症并不孕患者腹腔淋巴细胞及其白细胞介素-2的变化[J]。中华妇产科杂志,1998,33：17-19.
[5]CHAOUAT G,MENU E,CLARK DA,et a 1.Control of fetal survival nival in CBA/2 mice by lymphokine therap[J].J Re prod Ferrol,1990,89:447-458.
[6]WEED JC,ARQUEMBOURG P C.Endometriosis:Call it produce all autoimmune response resulting in infertility?Cain Ob ster Gyne col,1980,23:885-893
[7]TARTAKOVSKY B,GOLD STEIN O,BROSH N.Colony-Stein-elating factor-1 blocks early pregnancy in mice[J].Biol Re prod,1991,44:906-912.
[8]Rana N.Braun DP,House R, et al.Basal and stimulated secretion of cytokines by peritoneal macrophages in women with endometriosis.Fer til Steil,1996;65:925-930.
[9]Ts udo T,Hamada T,lake T, et al.Altered gene expression and secretion of interleukin-6 in stromal cells droved from endometrial tissue[J].Fer til Steil,2000,73:1205-1211.
[10]Schroeder W,Garget R, Interleukin-6 receptor in peritoneal fluid and serum of patients with endometriosis [J].Cain Exp Obstet Gyne col,1996,23(1):10-14.
[11]朱剑飞,陈友国,杨伟文：子宫内膜异位症患者血清及腹腔液白介索-6的临床意义[J].江苏医药杂志,2004,5(30)：362-363.
[12]BERPUIST A,BRUSE C,CARLBERG M,et al.Interleukin I-beta,Interleukin-6 and tumor necrosis factor-alpha in endomorphic fid due and in endometrium[J].Fer til Steil,2001, 5:489-495.
[13]Bedawin MA,Falcon T, et al.Prediction of endometriosis with serum and peritoneal fluid markers:a prospective controlled trial [J].Hum Record,2002,Fed,17(2):426-431.
[14]Song M,Carabine SA,Taradiddle N,et al.Presence of endometrial epithelial cell in the peritoneal cavity and the mesothelial inflammatory response[J].Fer til Steil,2003,79(Suppl 1):789-794.
[15]Barca E,Rozzer ES,Kolinski E et al.Angiogenic activity and IL-8 concentrations in peritoneal fluid and sers in endometriosis [J] Intt Gynecologic Obstet,2002,79(3):229-235.
[16]Aubergiste A,Netty H,Saffrony B, et al.Production of interleukins 1 beta,6 and 8 and tumor necrosis factor alpha in separated and cultured endometrial and endometrial stromal and epithelial cells.Gyne col Obstet Invest,2000;50(1):1-6.
[17]Vader Linden PJ.Theories on the pathogenesis of endometriosis.Hum Re prod,1996, 11:53-65.
[18]Lunisolar M,Casabas-Roux F, Donne J.Early stage endometriosis:adhesion and growth of human menstrual endometrium in nude mice. Fer til Steil,2000,74:306-312.
[19]Primula N,Saluda A,Epiloguize-Kalispel O, et al.Regulation of endometrial stromal cell matrix metropolitanate activity and invasiveness by interleukin-8. Fer til Steil,2004, 81:904-911.
[20]Galvani R,Smith L,Fowler PA.Effect of interleukin-8,anti-IL-8, and IL-12on endometrial cell survival in combined endometrial gland and stromal cell cultures derived from women with and without endometriosis. Fer til Steil,2002.Jan;77(1):62-70.
[21]Bacchante R,Bugler M,Touraine JL, et al.High levels of interleukin-10 production in vivo are associated with tolerance in patients transplanted with HLA mismatched hematopoietic stem cells.J Exp Med,1994; 179:493-502.
[22]Puniness J,Isolate K,Rasta H,et al,Increased levels of interleukin-6 and interleukin-10 in peritoneal fluid of patients with endometriosis.Am J Obstet Gyne col,1996; 174(5): 1522-1526.
[23]Biwabik T, Hamada T,et al.Tumor necrosis factor-alpha Promotes proliferation of endometrial stromal cells by inducing interleukin-8 gene and protein expression[J].Cline Endocrinal Meta,2000,85(2):824-829.
[24]林俊,张信美,邓琳,等.子宫内膜异位症患者血清和腹腔液中自细胞介素-2,1,6的检测[J].浙江大学学报(医学版),2005,34(3)：161-163.
[25]Con ti P,Tempura D,Dander K,et al. Interleukin-16 network in inflammation and allergy[J].Allergy Asthma Proc,2002,23(2):103-108.
[26]Amici A,Mesotheliomata I.Glutenous A,et al.Increased level of interleukin-15 in the peritoneal fluid of women with endometriosis:inverse correlation with stage and depth of invasion[J].Hum Re prod,2003,18(2):429-432.
[27]Roku H,Tsuris Y,Krishnamurti SI,et al.Role of interleukin-18 in pathogenesis of endometriosis[J]. Hum Re prod,2004,19(3):709-714.
[28]Aria A,Mesotheliomata I,Noumenon, et al. Altered expression of interleukin-18 in the peritoneal fluid of women with endometriosis[J]. Fer til Steil,2003,80(4):889-894.
[29]Aba Y, Hamada T,Horae S, et al.Lipopolysaccharide-promoted proliferation of densitometric stromal cells via induction of tumor necrosis factor alpha and interleukin-8 expression[J]. Fer til Steil,2004,82[Suppl3]:1036-1042.
[30]Bergama A,Burse C,Carl berg M, et al. interleukin-6 and tumor necrosis factor in endometrium [J]. Fer til Steil,2001,75:489-495.
[31]Phillips DG,Stone AM,Jones BD, et al.Vascular permeability factor(rhVEGF165) stellulate direct angiogenesis in the rabbit cornea in vivo.At tiki,1994;8:961-965.
[32]Park JE,Keller GA,Ferrara N.The vascular endothelial growth factor (VEGF) microfonns:differential deposition into the sub epithelial extracellular matrix and bioactivity of extracellular matrix-bound VEGF.Mol Biol cell,1993;4:1317-1324.
[33]Mahoe JL;Dago d MY;Han g JC Vascular endothelial growth factor and interleukin-6 in peritoneal fluid of women with endometriosis [J].Fer til Steil,2000,73(11):166-170.
[34]Reckoning PR;Kennedy SH;Bark ow DH.Endometrial disease:the role of peritoneal fluid[J].Hum Re pod Undate,1998,4(5):741-757.
[35]Biwabik T;Hamada T;Ts udo T Tumor necrosis factor-alpha promotes proliferation of endometrial stromal cells by inducing interleukin-8 gene and protein expression [J].J Cain Endorse Me tab,2000,85(2):824-829.
[36]蔡松园,赵淑萍.止痛化胶囊对子宫内膜异位症患者血清CA125及VEGF的影响[J].山东医药,2009,49(21)：77--78.
[37]Clarence J,Prentice A,Char nock-Jones DC,et al.Vascular endothelial growth factor concentrations are elevated in peritoneal fluid of women with endometriosis[J].Hum Re pod,1996;11(1):220-223.
[38]Bota T, Fuji I, Wana H, et al. Reduced HGF expression in subcutaneous C T26 tumor genetically modified to secrete NK4 and its possible relation with antitumor effects[J]. Cancer Sci,2004,95(4):321-327.
[39]Khan KN, Mikasuki H, Fuji A. et al. Peritoneal fluid and serum levels of hepatocyte growth factor may predict the activity of endometriosis[J]. Acta obstet Gyne col Sand,2006,85(4): 458-466.
[40]宗利丽,汀龙霞,赵军,等。干细胞生长因子及其受体在子宫内膜异位症动物模型的表达[J]。广东医学,2008,29(10)：1646-1648.-
[41]宗利丽,李亚里,哈小琴.子宫内膜异位症患者腹水与血清中肝细胞生长因子的检测[J].第一军医大学学报,2003,23(8)：757-759.
[42]宗利丽,李亚里,宋三泰,等.子宫内膜异位症患者肝细胞生长因子及其受体c-Met的表达[J].第一军医大学学报,2004,24(6)：619-621.
[43]闫桂英,郑慕白,章汉旺等.细胞间粘附分子-1在子宫内膜异位症患者在位内膜、腹腔液及异位病灶中的表达及分析.实用J妇产科杂志,2005,21：158-160.
[44]潘莉莉,秦伶,卢丽萍等.腹腔液中SICAM-1、TNF-a水平与子宫内膜异位症.中国优生与遗传杂志,2005,13：66-67.
[45]伍俊萍,张俊慧,刘银坤等.整合素B和细胞粘附分子在子宫内膜异位症在位内膜与异位内膜组织中的的表达.中华妇产科杂志,1999,34-204-206.
[46]徐兰芝,李亚里.子宫内膜异位症新标志物SIC AM-1的临床研究[D].北京：中国人民解放军军事进修学院硕十学位论文,2006.
[47]樊冬梅SICAM-1和CA125在子宫内膜异位症诊断中的意义[D].河南：郑州大学硕士学位论文,2006.
[48]Doghole TM,Miao L,Hill JA.Cytokine profiles in autologous peritoneal fluid and peripheral blood of women with dee and superficial endometriosis[J].Arch Gyne col Obstet,2001,265(1):41-44.
[49]Syllogize K,Kinetochore H,Banksia M, et al.The involvement of T lymphocytes in the pathogenesis of endometrial tissues overgrowth in women with endometriosis[J].Mediators Inflame,2003,12(3):131-138.
[50]王志萍,蔡呈香.血清cA125检测在妇科病临床应用的评价[J].海峡医学,2005,17(1)：61-63.
[51]金帆.子宫内膜异位症患者血清和腹水CA125水平测定[J].国外医学：妇产科分册,1995,22(2)：126.
[52]戚瑞珍,李亚里,关峥.CA125在子宫内膜异位症中的临床意义[J].中国妇幼保健,2007,22(26)：36443645.
[53]Danes AM, Irani K, Goldschmidt Clermont PJ, et al. A requirement for carl in the PDGF-stimulated migration of fibroblasts and vascular smooth cells[J].Biochemical Mol Biolint,1998,45(2):279-287.
[54]Inone K, Cynthia O, Kawabata Y, et al. Effect of BO-653 and protocol on c-myc and PDGF A messenger RNA of the artery after balloon denudation in cholesterol-fed rabbits[J]. Atheroscleroses,2002,161(2):353-363.
[55]Latchkey MW. Schlitz A. Volar B, et al. Combined inhibition of vascular endothelial growth factor(VEGF), fibroblast growth factor and platelet derived growth factor, but not inhibition of VEGF alone, effectively suppresses an-Gio-genesis and vessel maturation in endometriosis lesions[J]. Hum Re prod,2006,21(1):262-268.
[56]Overton C. Fernandez Shaw S, Hicks B, el al. Peritoneal fluid cytokines and the relationship with endometriosis and pain[J]. Hum Re prod,1996,11(2):380-386.
[57]Tutelage M, Lauren J, Berg sten E, et al. Chromosomal location, ex on structure, and vascular expression patterns of the human PDGFC and PDGFD genes[J]. Circulation, 2001,103(18):2242-2247.
[58]闫华,许俊华,郭淑青等.子宫内膜异位症患者血清及腹腔液中血小板衍生生长因子,血.管细胞粘附分子水平的变化及其意义.[J].生殖医学杂志,2008,17(5)；342-345.
[59]Bhang L, Yang N. Tumor—derived Vascular En dot Belial Growth Favor Up—regulates erythropoietin blood vessels-2 in Host En Doth Ilium and Destabilizes Host Vasculature, Supporting Angiogenesis in Ovarian Cancer[J]. Cancer Research,2003,63(12): 3403-3412.
[60]Goren H, Animistic K, Ivan K, et al. FGF-1 and SIOOA 13 Possibly Contribute to Angiogenesis in all endometrioses[J]. J Re prod Immunology,2005,67(1/2):87-101.
[61]Saite M, Hamadryas M, Shibuichi M, et al. Induction of Tube Formation by Angiotensin Endothelial Cell/FI bioblast Coculture Is Dependent on Endogenous VEGF[J]. Cancer Science,2003,94:782-790.
[62]Gill KA, Brindle NP. Angiotensin-2 Stimulates M ignition of En-endothelia Progenitors and Their Interaction with Endothelium[J]. Bio chem Bio phys Res Commune,2005, 336(2):392-396.