摘要
目的:观测子宫肌瘤大鼠模型的病理改变来探讨子宫肌瘤的病因机制。方法:将20只大鼠随机分为2组:正常对照组、模型组。采用雌、孕激素负荷法建立大鼠子宫肌瘤模型,观察大鼠子宫大体形态;HE染色镜下观察大鼠子宫平滑肌病理改变;镜下测量子宫平滑肌厚度,运用免疫组织化学检测方法来观察雌激素和孕激素在局部平滑肌的反应。结果:雌、孕激素负荷造模后,大鼠子宫大体观子宫色泽晦暗,明显肿胀、结节;镜下观察大鼠子宫平滑肌增生,细胞排列紊乱;平滑肌增厚,部分呈瘤样增生。两组局部ER、PR检测存在显著差异。结论:镜下观察大鼠模型组的子宫有平滑肌瘤形成,雌、孕激素负荷法大鼠子宫肌瘤模型成功建立。子宫平滑肌瘤形成的病因机制中,雌、孕激素起重要作用,而且跟局部平滑肌对雌、孕激素的敏感性密切相关。
Objective:To probe into the etiological mechanism of hysteromyoma by observing pathological changes in the model of hysteromyoma in rat.Methods:Divide 20 rats into two groups at random: a normal matched group and a model group. Create the model of hysteromyoma in rat by critical loads approach of estrogen and progestational hormone. Observe the gross morphological features of the hystera. Observe the pathological changes of the uterine smooth muscle of the rat with the HE microscope. Measure the thickness of the uterine smooth muscle. Observe the reaction of smooth muscle to estrogen and progestational hormone with immunohistochemical method.Results: After critical loads of estrogen and progestational hormone are molded, the gross morphological features of the hystera are dark and gloomy in color with obvious tumefaction and tuber. Uterine smooth muscle hyperplasia can be observed with disorder of cell arrangement. Uterine smooth muscle incrassation can also be observed with part of it resembling tumor. There is much difference between two groups of rats in ER and PR inspection.Conclusion:Through microscope observation, uterine smooth muscle tumor is seen to form in the model group of rats. Thus estrogen, progestational hormone critical loads approach rat hysteromyoma model has been created successfully. Estrogen and progestational hormone play an important role in the etiological mechanism of uterine smooth muscle tumor formation. This is closely related to the sensibility of local smooth muscle to estrogen and progestational hormone.
出处
《现代生物医学进展》
CAS
2010年第3期466-469,共4页
Progress in Modern Biomedicine
关键词
雌、孕激素
子宫肌瘤
动物模型
病因机制
estrogen
progestational hormone
hysteromyoma
animal model
etiological mechanism