寿胎丸对控制性超排卵小鼠子宫内膜血管内皮生长因子及其受体的影响研究

目的探讨寿胎丸提高控制性超排卵(Controlled Ovarian Hyperstimulation,COH)小鼠子宫内膜容受性的作用机制。方法采用促性腺激素释放激素激动剂+血清促性腺激素+人绒毛膜促性腺激素建立COH小鼠模型,将其分为模型组、寿胎丸高、中、低剂量组、阿司匹林对照组、同时设正常对照组,在造模的同时,寿胎丸高、中、低剂量组分别按6、3、1 g/kg寿胎丸灌胃;阿司匹林对照组按0.2 g/kg阿司匹林灌胃;模型组、正常对照组以等体积生理盐水灌胃,1次/d,连用11 d。采用HE染色、免疫组化法对子宫进行病理切片制作,通过Mias-2000图像分析系统检测子宫内膜血管内皮生长因子(Vascular Endothelial Growth Factor,VEGF)、血管内皮细胞生长因子受体-1(Vascular Endothelial Growth Factor Receptor-1,VEGFR-1)蛋白表达水平,并测量子宫内膜厚度及其血管数。结果与正常对照组比较,模型组、寿胎丸高、中、低剂量组、阿司匹林对照组子宫内膜厚度无明显变化;模型组子宫血管数、内膜VEGF、VEGFR-1明显减少(P0.05)。与模型组比较,寿胎丸高、中、低剂量组、阿司匹林对照组子宫血管数、内膜VEGF明显增多(P0.05),寿胎丸高剂量组、阿司匹林对照组子宫内膜VEGFR-1明显增多(P0.05)。结论寿胎丸可能通过促进COH小鼠子宫内膜VEGF及受体表达、增加子宫血管数量,进而提高COH小鼠子宫内膜容受性。

Study on effect of Shou Tai Wan on endometrial vascular endothelial growth factor and its receptor in controlled ovarian hyperstimulation mice

Objective To explore the mechanism of Shou Tai Wan in improving endometrial receptivity in controlled ovarian hyperstimulation ( COH) mice. Methods Established COH mice model by using gonadotropin releasing hormone agonist+ pregnant mare serum gonadotropin+ human chorionic gonadotropin ( GnRHa + PMSG + HCG) and divided them into 6 groups i. e. model group, high dose, medium dose and low dose Shou Tai Wan groups, aspirin control group and normal control group. While mice modeling, administrated Shou Tai Wan to high, medium and low dose groups (6g, 3g, 1 g/kg) IG respectively;aspirin (0. 2 g/kg) to aspirin group and 0. 9% saline to the model group and normal control group by the same way, once a day for 11 days. Observed uterine pathological sections with HE and immunohistochemical method, detected endometrial vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor -1(VEGFR - 1) protein expression level and measured the endometrial thickness and uterine vessels by Mias-2000 image analysis system. Results Compared with normal control group, no obvious change in endometrial thickness was found in the model group, Shou Tai Wan high, medium and low dose groups and aspirin group. The number of uterine vessels, endometrial VEGF and VEGFR-1 significantly reduced in the model group than that of normal control group (P<0. 05). The number of uterine vessel, endometrial VEGF significantly increased in high, medium and low dose Shou Tai Wan groups and aspirin group than that of the model group(P<0. 05). Endometrial VEGFR-1 significantly increased in high dose Shou Tai Wan group and aspirin group ( P <0. 05 ) . Conclusion Shou Tai Wan improves endometrial receptivity in COH mice through promoting endometrial VEGF and receptor expression and increasing the number of uterine vessels.