It is difficult to recruit patients.

NF-κB pathway activation-induced endometrial insulin resistance was one of the causes of infertility patients with PCOS and insulin resistance whose endometrial receptivity is declined .The investigators' previous findings indicated that the use of modified utral-long protocols ( GnRH-a was used twice in mid-luteal phaes) can improve clinical outcomes by improving endometrial receptivity in patients with PCOS , but the mechanism was not clear. Previous research also found that GnRH-a reduced the activity of NF-κB pathway in endometrial stromal cells and depended the dose and time.Thus, The investigators' subject will try to applicate GnRH-a to explore the influence of NF-κB pathway activity 、the state of insulin resistance and embryo implantation rate ;then we will investgate GnRH-a whether reduce NF-κB pathway activity-induced insulin resistance and ultimately improve endometrial receptivity by using GnRH-a in infertility patients with PCOS and insulin resistance.The investigators' research attempt to provide ideas for seeking inflammatory medication target in assisted reproductive technology in patients with PCOS by exploring the immune mechanism of GnRHa on improving the endometrial receptivity .

The endometrial biopsy was performed in the previous cycle of the protocol. According to the expression of NF-κB in the endometrium random group. The difference of NF - κB expression in patients with different protocol were compared.

Inclusion Criteria:

• age<36years,
• PCOS,
• Insulin resistance (HOMA-IR = fasting insulin (FINS) × fasting blood glucose (FPG) / 22.5, HOMA-IR ≥ 2.69 ）;

Exclusion Criteria:

• uterine abnormalities (double uterus, bicornuate uterus, unicornuate uterus and uterine mediastinum),
• intrauterine adhesions,
• endometriosis, adenomyosis,
• Hydrosalpinx,
• uterine fibroids (submucosal fibroids, non-mucosal fibroids > 4 cm and / or endometrial pressure),
• Hyroid dysfunction and hyperprolactinemia.