Abstract
A chronic low-grade inflammation state accounts for an important part of the pathogenesis of polycystic ovary syndrome (PCOS). The adipose tissue derived cytokine chemerin has recently been proven to be a proinflammatory chemokine, but its mechanism involved in the pathogenesis of PCOS remains largely unresolved. From non-obese patients with and without PCOS, follicular fluid and granulosa cells were retrieved. The effect of testosterone on the expression of chemerin and its receptors was explored in granulosa cells. IVF outcomes in different groups based on FF-chemerin (chemerin in the follicular fluid) level were further compared. The concentration of FF-chemerin, and the mRNA expression of chemerin and its receptors in granulosa cells from PCOS were significantly higher than those from non-PCOS. FF-chemerin was positively correlative to total testosterone (TT) and luteinizing hormone (LH) in the follicular fluid. Furthermore, testosterone upregulated the expression of chemerin and its receptors in vitro. The oocyte utilization rate and high-quality embryo rate were significantly decreased in the high FF-chemerin group. The upregulated chemerin levels in the ovary of PCOS patients, which may be caused by ovarian hyperandrogenism, may be a risk factor for oocyte maturation and embryo development. These findings may provide a basis for novel interventions to improve IVF outcomes.
摘要
慢性轻度炎症状态是多囊卵巢综合征(PCOS)发病机理的重要组成部分。脂肪组织来源的细胞因子chemerin最近被证明是促炎性趋化因子, 但其参与PCOS发病机理的机制仍未明确。从PCOS和非PCOS非肥胖患者中, 获取卵泡液和颗粒细胞。在颗粒细胞中检测睾酮对chemerin及其受体表达的影响。根据FF-chemerin(卵泡液中的chemerin)水平, 比较不同组的IVF结局。 PCOS患者的颗粒细胞中FF-chemerin的浓度以及chemerin及其受体的mRNA表达明显高于非PCOS患者的颗粒细胞。 FF-chemerin与卵泡液中的总睾酮(TT)和黄体生成激素(LH)呈正相关。此外, 睾酮在体外上调了chemerin及其受体的表达。高FF-chemerin组的卵母细胞利用率和优质胚胎率显着降低。 PCOS患者卵巢中chemerin水平的升高可能是卵巢高雄激素血症引起的, 可能为卵母细胞成熟和胚胎发育的危险因素。这些发现可能为改善IVF结局的新干预措施提供基础。
The Chinese abstracts are translated by Prof. Dr. Xiangyan Ruan and her team: Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100026, China.
Disclosure statement
The authors have no conflicts of interest to disclose.