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Objective: SD rats by ligation of the uterine artery, an animal model to build thin endometrium and endometrial rats after chronic ischemic endometrial thickness, changes in the number of endometrial glands, simultaneous detection of telomerase (TERT), POU5f1, c-kit expression and caspase3. Methods: Healthy female 6-8 weeks old SD rats weighing 180-200 g, by the Experimental Animal Center of Chongqing Medical University. Rats were randomly divided into two groups: sham operation group (control group), bilateral uterine artery ligation group (experimental group), each 30. The use of 10% chloral hydrate intraperitoneally (0.3mL/100g) anesthetized rats, and then sit on the mounting plate, abdomen after disinfection, abdominal incision to expose the uterus, uterine horn artery ligation, and then close the abdominal cavity. Sham braid without ligation, and then close the abdominal cavity. Rat vaginal smears judged through sexual cycle, after three months, the rats were sacrificed at estrus uterine tissue stored in liquid nitrogen tank. Stored at -70 ° C so the organization. In the light microscope view of endometrial tissue microstructure changes in endometrial thickness measurement, the thickness of luminal epithelium, glandular epithelial thickness, number of endometrial glands and endometrial glands volume fraction. And the use of immunohistochemical techniques and caspase3 telomerase expression; fluorescence quantitative PCR c-kit, POU5f1 and caspase3 expression; western blot detection of telomerase, c-kit expression and caspase3. Results 1 and the control group, model group endometrial thickness (502 ± 148), luminal epithelium thickness (17.20 ± 4.98), glandular epithelial thickness (9.17 ± 1.96), the number of endometrial glands (18.9 ± 4.8) and endometrial gland volume fraction (0.15 ± 0.02) and control group intimal thickness (800 ± 130), luminal epithelium thickness (29.46 ± 9.27), glandular epithelial thickness (15.68 ± 2.50), the number of endometrial glands (30 ± 5.5) and endometrial glands volume fraction (0.40 ± 0.16) were significantly lower compared (P lt; 0.05). (2) the model group c-kit mRNA and protein levels [(0.235 ± 0.012), (0.31 ± 0.13)] compared with the control group [(1 ± 0.063), (0.75 ± 0.09)] was significantly lower (P lt; 0.05); protein levels (0.64 ± 0.19) was significantly lower than the control group (0.87 ± 0.12) (P lt; 0.05); model group and control group POU5f1 mRNA, the difference was not significant (P gt; 0.05). Conclusion 1 SD rats by ligation of the uterine artery can build endometrial chronic ischemic injury model. 2 endometrial pathology of chronic ischemic injury and clinical pathology consistent with thin endometrium, can serve as a good animal model for thin endometrium. 3 endometrial chronic ischemia and chronic ischemia-induced endometrial telomerase and c-kit downregulation, caspase3 increased expression of thin endometrium may be a factor in pathogenesis.
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