加减苍附导痰汤对PCOS模型大鼠子宫内膜GLUT4表达的影响

Effect of Modified Cangfu Daotan Decoction on Expression of GLUT4 in Endometrium of Rats with Polycystic Ovary Syndrome

目的:探讨加减苍附导痰汤对多囊卵巢综合征(PCOS)大鼠子宫内膜容受性的影响。方法:85日龄SD雌性大鼠随机分出空白对照组15只,余大鼠参照Poresky造模方法,采用胰岛素(INS)联合绒促性素(HCG)复制符合多囊卵巢综合征临床血清激素水平、卵巢形态改变的肥胖PCOS大鼠模型,分为模型组、二甲双胍组、加减苍附导痰汤组各15只,分别ig生理盐水、二甲双胍(0.135 g.kg-1)及加减苍附导痰汤(15.84 g.kg-1),连续14 d。观察对各组大鼠子宫内膜葡萄糖转运因子4(GLUT4),胰岛素(INS)及其受体(INS-R)的影响。结果:模型组子宫内膜腺上皮GLUT4,INS-R表达明显低于空白对照组(P<0.05),模型组INS表达明显高于空白对照组(P<0.05);加减苍附导痰汤组、二甲双胍组GLUT4,INS-R表达明显高于模型组(P<0.05),与空白对照组比较已无明显差异。加减苍附导痰汤组、二甲双胍组INS表达明显低于模型组(P<0.05),与空白对照组比较已无明显差异。结论:加减苍附导痰汤可增加GLUT4,INS-R在子宫内膜组织的表达,改善子宫内膜INS-R缺陷和胰岛素抵抗(IR),提高子宫内膜对葡萄糖的利用,从而增加内膜容受性。

Objective：To study the effect of modified Cangfu Daotan decoction （CDD） on endometrial receptivity in rats with polycystic ovary syndrome（PCOS）. Method： Female rats of 85 days were selected as the control group. The other rats were induced by Poretskyp＇s method for PCOS model, and then were randomly divided into model group, metformin treatment group （0.135 g·kg-1）, and CDD group （15.84 g·kg-1） respectively. After 14 days of treatment, the rats were killed, and the expression of glucose transporter 4（GLUT4）, insulin（INS）, insulin recptor（INS-R） in endometrium were detected. Result： GLUT4 and INS-R of endometrial glandulan epithelium in PCOS model group were significantly lower than those in control group（P〈0.05）, INS in PCOS model group were significantly higher than that in control group（P〈0.05）; GLUT4 and INS-R in CDD group and metformin treatment group were significantly higher than those in PCOS model group（P〈0.05）,and had no significant difference with those in control group.INS in CDD group and metformin treatment group were significantly lower than those in PCOS model group（P〈0.05）, and had no significant difference with those in control group. Conclusion： CDD can increase expression of GLUT4, INS-R in endometrial tissue, improve endometrial defects of INS-R and IR, improve endometrial on glucose utilization, thereby increasing the endometrial receptivity.