Inducing malignant transformation of endometriosis in rats by long-term sustaining hyperestrogenemia and type II diabetes.
Inducing malignant transformation of endometriosis in rats by long-term sustaining hyperestrogenemia and type II diabetes.
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长期维持高雌激素血症和II型糖尿病诱导大鼠子宫内膜异位症恶变
DOI：
10.1111/cas.12573
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发表时间：
2015-01
期刊：
影响因子：
5.7
通讯作者：
Ren F
中科院分区：
文献类型：
--
作者：
Wang CT;Wang DB;Liu KR;Li Y;Sun CX;Guo CS;Ren F
本研究旨在通过高雌激素血症和II型糖尿病诱导Sprague-Dawley大鼠子宫内膜异位症恶变，并评估其与人类疾病在生物学特征上的相似性。手术诱发子宫内膜异位症的大鼠被随机分为两组：接受雌二醇（5 mg/kg，术后每周 3 次）、链脲佐菌素（25 mg/kg，术后 1 个月）和高碳水化合物和脂肪饲料治疗的组（Es 组）；以及用安慰剂盐水和标准饲料治疗的组（对照组）。所有大鼠在手术后 2、4 或 8 个月被随机处死。对子宫内膜异位病灶和相应的在位子宫内膜进行形态学评估、TUNEL和免疫组化分析增殖细胞核抗原、磷酸酶和张力蛋白同源物、磷酸化蛋白激酶B和磷酸化哺乳动物雷帕霉素靶蛋白的表达。 Es组中，3例（6.0%）子宫内膜异位症表现为不典型增生，伴有单纯增生性在位子宫内膜，2例（4.0%）子宫内膜异位症表现为子宫内膜样癌，伴有不典型增生性在位子宫内膜。 Es组细胞器活性及增殖细胞核抗原、磷酸化蛋白激酶B、雷帕霉素磷酸化哺乳动物靶点表达升高，磷酸酶、张力蛋白同源物水平及TUNEL阳性程度按子宫内膜异位症、非典型子宫内膜异位症、恶性子宫内膜异位症的顺序依次降低。在相应的在位子宫内膜中也发现了相同的趋势。诱发的恶性子宫内膜异位症在病理过程、组织形态学和分子生物学特征上与人类疾病有相似之处。该方法是可行的。子宫内膜异位症和在位子宫内膜的恶变可能具有相关性和相似性，但前者癌变的风险可能更高。
This study aimed to induce malignant transformation of endometriosis in Sprague–Dawley rats by hyperestrogenemia and type II diabetes and evaluate its similarity with human disease in biological features. Rats with surgically induced endometriosis were randomized into two groups: those treated with estradiol (5 mg/kg three times/week after surgery), streptozotocin (25 mg/kg, 1 month after surgery), and high carbohydrate-and-fat feed (Es group); and those treated with placebo saline and standard feed (control group). All rats were randomly killed 2, 4, or 8 months after surgery. The endometriosis lesions and the corresponding eutopic endometria were subjected to morphological evaluation, TUNEL, and immunohistochemical analysis for the expressions of proliferating cell nuclear antigen, phosphatase and tensin homolog, phosphorylated protein kinase B, and phosphorylated mammalian target of rapamycin proteins. In the Es group, three cases (6.0%) of endometriosis showed atypical hyperplasia accompanied by simple hyperplastic eutopic endometria, and two cases (4.0%) of endometriosis showed endometrioid carcinoma accompanied by atypical hyperplastic eutopic endometria. In the Es group, the activity of organelles and the expressions of proliferating cell nuclear antigen, phosphorylated protein kinase B, and phosphorylated mammalian target of rapamycin increased, and the level of phosphatase and tensin homolog and TUNEL positivity decreased progressively in the order of endometriosis, atypical endometriosis, and malignant endometriosis. The same tendency was found in the corresponding eutopic endometria. The induced malignant endometriosis showed similarities with human disease in the pathological process and histomorphological and molecular biological features. The method is feasible. The malignant transformations of endometriosis and eutopic endometria may have correlations and similarities, but the former may suffer a higher risk of canceration.
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