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张璐,李莹,吕晓丹,苏兴,马旭,夏红飞.2017.大鼠子宫宫腔粘连模型的建立及评价指标.动物学杂志,52(1):115-121.
大鼠子宫宫腔粘连模型的建立及评价指标
Establishment and Evaluation of Rat Model with Intrauterine Adhesions
投稿时间:2016-03-30  修订日期:2016-11-11
DOI:10.13859/j.cjz.201701013
中文关键词:  大鼠  子宫内膜损伤  动物模型  评价指标
英文关键词:Rat  Endometrial injury  Animal model  Evaluation indicator
基金项目:国家自然科学基金项目(No. 81370720)和中央级公益性科研院所基本科研业务费专项(No. 015GJZ01);
作者单位E-mail
张璐 ①国家卫生计生委科学技术研究所遗传优生中心
②北京协和医学院研究生院 
ZLu7649@163.com 
李莹 ①国家卫生计生委科学技术研究所遗传优生中心
②北京协和医学院研究生院 
 
吕晓丹 ①国家卫生计生委科学技术研究所遗传优生中心
②北京协和医学院研究生院 
 
苏兴 ①国家卫生计生委科学技术研究所遗传优生中心
②北京协和医学院研究生院 
 
马旭 ①国家卫生计生委科学技术研究所遗传优生中心
②北京协和医学院研究生院 
 
夏红飞* ①国家卫生计生委科学技术研究所遗传优生中心
②北京协和医学院研究生院 
hongfeixia@126.com 
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中文摘要:
      子宫内膜损伤是导致宫腔粘连的最主要原因,建立有效的子宫内膜损伤动物模型是研究此类疾病发生、发展和治疗反应等不可或缺的支撑条件。通过宫腔注射95%的乙醇制造大鼠(Rattus norvegicus)子宫内膜损伤模型,检测胚胎植入数目来分析子宫内膜损伤对大鼠生育情况的影响,观察大鼠子宫内膜厚度、腺体数量和纤维化面积,分析乙醇处理对子宫内膜的影响;检测细胞角蛋白(CK-19)和波性蛋白(Vimentin)的表达水平,分析上皮细胞和间质细胞的增殖分化及子宫内膜损伤程度。结果显示,正常组大鼠子宫比损伤组更为平滑且有韧性,与正常组相比,损伤组大鼠生育率显著降低(P < 0.01),子宫内膜厚度变薄(P < 0.01)、腺体数量显著减少(P < 0.01),纤维化面积显著增大(P < 0.01),CK-19和Vimentin表达量显著下调。结果提示已成功建立大鼠子宫内膜损伤动物模型。
英文摘要:
      Endometrial lesion is the main reason leading to cervical adhesion. Establishing an effective animal model of endometrial injury is an indispensable condition to study the disease occurrence, development and treatment. We established a Rat (Rattus norvegicus) model of endometrial injury by intrauterine injection of 95% alcohol. The numbers of embryo implantation were detected to analyze the effect of endometrial injury on the fertility. The thickness of endometrium, gland numbers and the area of fibrosis were observed to analyze the effects of ethanol treatment on the endometrium. The expressions of cytokeratin 19 (CK-19) and Vimentin were detected to analyze the status of epithelium and mesenchymal cells. The results showed that the specimen of Rat uterus in normal group was smooth and showed strong toughness compared with injury group, and the fertility in the injury group was significantly lower than that in control group (P < 0.01) (Fig. 1). Rat endometrium in the injury group was much thinner than that in control group (P < 0.01) (Fig. 2e). Moreover, compared with control group, the gland numbers in the injury group was significantly reduced (P < 0.01) (Fig. 2f), the area of fibrosis was increased (P < 0.01) (Fig. 2g) and the expression of CK-19 and vimentin was remarkably decreased (Fig. 3). The results suggest that the animal model of Rat endometrial injury is successfully established.
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