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目的:探讨瘦素及瘦素信号传导系统中各关键信号蛋白在子宫内膜的表达及其调控。方法:健康雌性B6.Cg-m+/+Leprdb小鼠(实验组)和其同窝出生的雌性野生型C57BL/6J小鼠(对照组)各10只,于16周龄的动情间期进行瘦素刺激实验,用免疫组化法检测瘦素及瘦素信号传导系统中各关键信号蛋白在子宫内膜的表达情况。结果:①16周龄时与对照组比,实验组较其体重增加约1倍(P<0.01),性腺周围脂肪垫重量增加约10倍(P<0.01);血葡萄糖、低密度脂蛋白胆固醇(LDL-C)和胰岛素水平增加2-3倍(P<0.01);子宫重量及E2、P、FSH、LH水平显著下降(P<0.05)。阴道涂片发现对照组均出现正常的动情周期,而实验组则始终处于动情间期。②免疫组化研究显示,瘦素信号传导系统的各关键信号蛋白在对照组子宫内膜间质中均有表达,但在子宫瘦素受体缺失组则JAK2为阴性表达,stat3的磷酸化过程也受阻。结论:①瘦素对子宫内膜存在影响。②体内瘦素受体缺失引起机体的高糖脂血症导致了子宫的脂质化,同时子宫局部的瘦素信号传导缺失,均可能参与生殖功能障碍。
Objective: To investigate the expression and regulation of key signaling proteins in leptin and leptin signaling system in the endometrium. Methods: Ten healthy female B6.Cg-m + / + Leprdb mice (experimental group) and 10 female wild-type C57BL / 6J mice (control group) Stimulation experiments were performed to detect the expression of key signaling proteins in leptin and leptin signaling system in the endometrium by immunohistochemistry. Results: Compared with the control group, the body weight of the experimental group increased about 1 time (P <0.01) and the weight of the fat pad around the gonads increased about 10 times (P <0.01) at 16 weeks of age. The blood glucose, LDL cholesterol LDL-C) and insulin levels increased 2-3 times (P <0.01). The uterine weight and the levels of E2, P, FSH and LH were significantly decreased (P <0.05). Vaginal smears found that the control group were normal estrous cycle, while the experimental group is always in the period of estrus. ② Immunohistochemical studies showed that the key signaling proteins of leptin signaling system were expressed in the control group of endometrial stroma, but in the uterine leptin receptor-deficient group, JAK2 was negatively expressed, the phosphorylation of stat3 Also blocked. Conclusion: ① Leptin has an effect on the endometrium. ② body leptin receptor deficiency caused by the body’s hyperlipidemia led to the uterine lipidation, while the uterine leptin signal transduction is missing, may be involved in reproductive dysfunction.