Cummings A M, Metcalf J L
Endocrine Branch, NHEERL, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA.
Proc Soc Exp Biol Med. 1996 Sep;212(4):332-7. doi: 10.3181/00379727-212-44022.
Endometriosis, a disease of women and nonhuman primates in which endometrial tissue grows outside the uterus, can be mimicked surgically in rats and mice. The disease is related to infertility in women, and surgical induction of endometriotic lesions reduces fertility in rats according to some studies. Conversely, pregnancy appears to have a beneficial effect on endometriosis in women and some rat studies. Our objective was to evaluate a new mouse model of surgically induced endometriosis with respect to the effects of pregnancy on endometriosis and the effects of endometriosis on pregnancy. Female B6C3F1 mice were divided into four groups. Those in Group A and B underwent induction surgery for endometriosis and hemi-ovariectomy, those in Group C underwent sham surgery and hemi-ovariectomy, and animals in Group D received no surgery at all. Three weeks later, Group A, C, and D were bred. Eighteen days later one half of the dams in Groups A, B, and C only were sacrificed, and evaluations included endometriotic lesion diameter, number of pups, fetal weight, and various organ weights. The remaining dams delivered, and, 18 days after parturition, dams and pups were sacrificed. Evaluations included gestation length and those listed above. Endometriotic lesion diameter was significantly reduced in pregnant animals when compared with nonpregnant controls, but the reduction was not a full regression. Lactation returned the mean lesion diameter to pre-pregnancy dimensions. When effects of endometriosis on pregnancy were evaluated, no effects on the litter size, pup weight, or gestation length were found, but trends toward increased resorptions and malformations were evident. Thus, in the mouse model of induced endometriosis, pregnancy produced a significant reduction in endometriotic lesion diameter while fertility was largely unaffected by the surgically induced endometriosis. The mouse model of endometriosis thus appears more resistant than the rat model to effects of endometriosis on fertility.
子宫内膜异位症是一种女性和非人灵长类动物的疾病,其特征是子宫内膜组织生长在子宫外,这种疾病可以通过手术在大鼠和小鼠身上模拟出来。该疾病与女性不孕有关,一些研究表明,手术诱导的子宫内膜异位病变会降低大鼠的生育能力。相反,怀孕似乎对女性子宫内膜异位症有有益影响,一些大鼠研究也证实了这一点。我们的目的是评估一种新的手术诱导子宫内膜异位症小鼠模型,以研究怀孕对子宫内膜异位症的影响以及子宫内膜异位症对怀孕的影响。雌性B6C3F1小鼠被分为四组。A组和B组小鼠接受子宫内膜异位症诱导手术和半卵巢切除术,C组小鼠接受假手术和半卵巢切除术,D组小鼠不接受任何手术。三周后,A组、C组和D组小鼠进行繁殖。18天后,仅对A组、B组和C组中的一半母鼠进行处死,评估指标包括子宫内膜异位病变直径、幼崽数量、胎儿体重和各种器官重量。其余母鼠分娩,分娩后18天,对母鼠和幼崽进行处死。评估指标包括妊娠期长度以及上述指标。与未怀孕的对照组相比,怀孕动物的子宫内膜异位病变直径显著减小,但并未完全消退。哺乳使平均病变直径恢复到怀孕前的大小。在评估子宫内膜异位症对怀孕的影响时,未发现对窝仔数、幼崽体重或妊娠期长度有影响,但吸收增加和畸形的趋势明显。因此,在诱导性子宫内膜异位症小鼠模型中,怀孕使子宫内膜异位病变直径显著减小,而手术诱导的子宫内膜异位症对生育能力的影响在很大程度上未受影响。因此,子宫内膜异位症小鼠模型似乎比大鼠模型对子宫内膜异位症对生育能力的影响更具抵抗力。