Correlation between leptin and IFN-γ involved in granulosa cell apoptosis in PCOS

Abstract

Objectives

Our study aimed to explore the relationship between leptin and IFN-γ in PCOS patients, and confirmed the effect of leptin-induced IFN-γ on granulosa cells furtherly.

Methods

29 patients with PCOS and 36 healthy controls were enrolled. Leptin level and the proportion of Th1 cells were detected and association between them were analyzed. Meanwhile, peripheral blood mononuclear cells (PBMCs) isolated from PCOS patients were treated with leptin and then the proportion of Th1 was analyzed. Besides that, the apoptotic level of KGN cells was monitored after IFN-γ treatment.

Results

In the circulation of PCOS patients, leptin level dramatically increased compared with controls. And, this was associated with upregulated Th1 cells proportion and IFN-γ level. In vitro, Th1 cells proportion increased after leptin treated PBMCs from PCOS patients. Furthermore, for KGN cells, the percentage of live cells decreased and later apoptosis cells increased after IFN-γ treatment.

Conclusions

Our results indicated that leptin takes part in process of PCOS via inducing expression of IFN-γ. Our findings highlight the importance of the connection between leptin and inflammation in PCOS and provide new insights therapeutic strategy for this disease.

摘要

目的：本研究旨在探讨瘦素与干扰素-γ在多囊卵巢综合征（PCOS）患者中的关系, 进一步证实瘦素诱导的干扰素-γ对颗粒细胞的作用。

方法：检测了29例PCOS患者和36例健康对照血清瘦素水平和Th1细胞比例, 并进行相关性分析。同时, 分离PCOS患者外周血单个核细胞（PBMC）, 用瘦素处理, 分析Th1细胞比例。此外, 还检测了干扰素γ处理后KGN细胞的凋亡水平。

结果：PCOS患者瘦素水平较对照组显著升高, 而且, 这与Th1细胞比例和干扰素-γ水平上调有关。在体外, 瘦素处理PCOS患者PBMCs后, Th1细胞比例增加。此外, 经IFN-γ处理后, KGN细胞的活细胞百分率下降, 凋亡细胞百分率增加。

结论：我们的结果提示瘦素通过诱导干扰素-γ的表达参与了PCOS的发病过程。我们的发现强调了瘦素与PCOS炎症之间的重要性, 并为这种疾病提供了新的治疗策略。

Keywords:

• Leptin
• polycystic ovary syndrome
• inflammation
• granulosa cell apoptosis
• IFN-γ

Disclosure statement

The authors confirm no conflict of interests related to our study.

Additional information

Funding

This work was supported by Changzhou Science and Technology Bureau Project (YB2017315) and Wuxi Science and Technology Bureau Project (ZYZD201801).