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目的:观察补肾化痰方药与二甲双胍联合应用对多囊卵巢模型大鼠的干预作用,探讨联合用药对PCOS的部分作用机制。方法:23日龄雌性SD大鼠60只,随机分为6组:正常对照组,模型对照组,西药治疗组,中药高剂量组,中药低剂量组,联合用药组,每组10只。采用雄性激素诱导PCOS模型,然后分别给予补肾化痰方和(或)二甲双胍进行干预,连续给药15 d。采用ELISA法检测各组大鼠血清胰岛素含量,采用Western-blot法检测大鼠卵巢组织中胰岛素受体表达水平,采用RT-PCR法检测大鼠卵巢组织中胰岛素受体mRNA表达水平。结果:与空白对照组比较,其余各组大鼠血清胰岛素及卵巢组织中胰岛素受体mRNA及蛋白表达水平显著升高(P<0.01),与模型对照组比较,各治疗组血清胰岛素及胰岛素受体mRNA及蛋白表达水平显著下降(P<0.01),以中西药联用组下降最为明显。结论:该中药方剂能够显著抑制多囊卵巢大鼠模型血清胰岛素水平,同时能够降低胰岛素受体基因及蛋白表达水平,而中西药联用疗效更佳。其治疗机制可能是通过抑制血清胰岛素及卵巢组织中受体表达而实现的。
Objective: To observe the intervention of Bushen Huatan Recipe and metformin on the polycystic ovary model rats, and to explore the partial mechanism of the combination therapy on PCOS. Methods: Sixty female SD rats of 23 days old were randomly divided into 6 groups: normal control group, model control group, western medicine treatment group, high-dose Chinese medicine group, low-dose Chinese medicine group and combination therapy group. The model of PCOS was induced by androgen and then given to the patients with tonifying kidney and phlegm and / or metformin for continuous administration for 15 days. Serum insulin levels of rats in each group were detected by ELISA. The expression of insulin receptor was detected by Western-blot and the expression of insulin receptor mRNA in ovary tissue was detected by RT-PCR. Results: Compared with the blank control group, the levels of insulin receptor mRNA and protein in the serum insulin and ovarian tissue in the other groups were significantly increased (P <0.01). Compared with the model control group, the levels of serum insulin and insulin The level of mRNA and protein expression decreased significantly (P <0.01), with the combination of Chinese and Western medicine decreased the most obvious. Conclusion: The traditional Chinese medicine prescription can significantly inhibit the serum insulin level in the polycystic ovary model rats, reduce the expression of insulin receptor gene and protein at the same time, and the combination of the traditional Chinese and western medicine has a better curative effect. Its therapeutic mechanism may be through inhibiting serum insulin and ovarian tissue receptor expression achieved.