Braun Donald P, Ding Jianchi, Dmowski W Paul
Institute for the Study and Treatment of Endometriosis and Rush Medical College, Chicago, Illinois, USA.
Fertil Steril. 2002 Oct;78(4):727-32. doi: 10.1016/s0015-0282(02)03318-6.
To determine the effect of autologous peritoneal fluid and tumor necrosis factor-alpha (TNF-alpha) on proliferation of endometrial cells from women with endometriosis.
Endometrial cells from eutopic and ectopic endometrium were cultured in vitro with peritoneal fluids or recombinant TNF-alpha for 72 hours before DNa synthesis determination by 3H-thymidine labeling and liquid scintillation counting.
An institute for the study and treatment of endometriosis and university-based research laboratories.
PATIENT(S): Thirty-five women with endometriosis and 17 controls without endometriosis.
MAIN OUTCOME MEASURE(S): In vitro incorporation of 3H-thymidine in endometrial cells was examined.
RESULT(S): Peritoneal fluid from women with endometriosis enhanced proliferation of autologous and heterologous endometrial cell cultures from women with endometriosis. The soluble TNF-receptor etanercept blocked the ability of peritoneal fluid from women with endometriosis to enhance proliferation of eutopic or ectopic endometrial cells. Recombinant TNF-alpha also enhanced proliferation of eutopic and ectopic endometrial cells from women with endometriosis. In contrast, autologous peritoneal fluid, heterologous peritoneal fluid from women with endometriosis, and recombinant TNF-alpha failed to enhance, and often inhibited, the proliferation of eutopic endometrial cells from controls without endometriosis.
CONCLUSION(S): Endometrial cells from women with endometriosis can utilize factors in peritoneal fluids, such as TNF-alpha, to facilitate proliferation in ectopic environments. Endometrial cells from women without endometriosis do not share this ability, suggesting that this abnormality is etiologically related to development of the disease. Therapy with agents that block the effects of TNF-alpha may be warranted.
确定自体腹腔液和肿瘤坏死因子-α（TNF-α）对子宫内膜异位症患者子宫内膜细胞增殖的影响。
在位内膜和异位内膜的子宫内膜细胞与腹腔液或重组TNF-α在体外培养72小时，然后通过³H-胸腺嘧啶核苷标记和液体闪烁计数法测定DNA合成。
一家子宫内膜异位症研究与治疗机构以及大学研究实验室。
35例子宫内膜异位症患者和17例无子宫内膜异位症的对照者。
检测³H-胸腺嘧啶核苷在子宫内膜细胞中的体外掺入情况。
子宫内膜异位症患者的腹腔液可增强来自子宫内膜异位症患者的自体和异体子宫内膜细胞培养物的增殖。可溶性TNF受体依那西普可阻断子宫内膜异位症患者腹腔液增强在位或异位子宫内膜细胞增殖的能力。重组TNF-α也可增强子宫内膜异位症患者在位和异位子宫内膜细胞的增殖。相比之下，自体腹腔液、子宫内膜异位症患者的异体腹腔液以及重组TNF-α均未能增强，且常抑制无子宫内膜异位症对照者在位子宫内膜细胞的增殖。
子宫内膜异位症患者的子宫内膜细胞可利用腹腔液中的因子（如TNF-α）促进异位环境中的增殖。无子宫内膜异位症患者的子宫内膜细胞不具备这种能力，提示这种异常在病因上与该疾病的发生有关。使用阻断TNF-α作用的药物进行治疗可能是必要的。
