Dexamethasone Restores the Repressive Effect of Tumor Necrosis Factor-α on Follicular Growth and E(2) Secretion During the In Vitro Culture of Preantral Follicles.
Dexamethasone Restores the Repressive Effect of Tumor Necrosis Factor-α on Follicular Growth and E(2) Secretion During the In Vitro Culture of Preantral Follicles.
复制标题
地塞米松恢复腔前卵泡体外培养过程中肿瘤坏死因子-α 对卵泡生长和 E2 分泌的抑制作用
DOI：
10.1007/s43032-021-00521-6
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发表时间：
2021-11
期刊：
影响因子：
--
通讯作者：
Li Z
中科院分区：
文献类型：
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作者：
Wu Q;Zhuang T;Li Z
肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）是一种促炎细胞因子，在女性生殖道中起重要作用，影响卵泡发育和子宫周期的各个阶段。高水平的TNF-α在多囊卵巢综合征（PCOS）患者的发病机制中起重要作用。临床医生认为地塞米松可以通过抑制肾上腺来抑制雄激素的诱导，从而改善PCOS患者的内分泌系统状态。我们推测地塞米松具有更多的功能，可以通过拮抗TNF-α发挥治疗作用。我们在卵泡培养液中加入TNF-α，以模拟PCOS患者内分泌环境中观察到的高TNF-α水平。在培养液中加入地塞米松，以确定其是否可以抵消TNF-α对卵泡生长和17β-雌二醇（E2）分泌的抑制作用。测量卵泡直径、E2浓度、卵泡存活率、窦状腔形成和排卵，以评估地塞米松的作用。在我们的研究中，TNF-α以剂量依赖的方式抑制体外卵泡生长和E2分泌。结论：地塞米松可部分抵消TNF-α对小鼠腔前卵泡体外培养中卵泡生长和E2分泌的抑制作用。因此，本文的研究结果表明，地塞米松可能通过抵消TNF-α在PCOS患者中的作用而作为治疗。这些结果为探索地塞米松治疗PCOS患者提供了新的依据。
As a proinflammatory cytokine, tumor necrosis factor-α (TNF-α) is central to the female reproductive tract and affects various phases of follicular development and uterine cycles. High levels of TNF-α play a vital role in the pathogenesis of polycystic ovary syndrome (PCOS) in patients. Clinicians know that dexamethasone can inhibit the induction of androgen by suppressing the adrenal glands which improves the status of the endocrine system in PCOS patients. We hypothesize that dexamethasone has much more functionality and can exert a therapeutic effect by antagonizing TNF-α. We added TNF-α to the follicular culture medium to simulate the high TNF-α levels observed in the endocrine environment of PCOS patients. Dexamethasone was added to the medium to determine if it could counteract the inhibitory effect of TNF-α on follicular growth and 17β-estradiol (E2) secretion. Follicular diameter, E2 concentration, follicle survival, antral-like cavity formation, and ovulation were measured to assess the effects of dexamethasone. In our work, TNF-α inhibited in vitro follicular growth and E2 secretion in a dose-dependent manner. Based on the results of the present research, we concluded that the addition of dexamethasone partially counteracts the repressive effect of TNF-α on follicle growth and E2 secretion during in vitro culture of the preantral follicles of mice. Thus, the findings in this paper suggest that dexamethasone may act as a therapy by counteracting the effects of TNF-α in PCOS patients. These results provide a new foundation for exploring the treatment of PCOS patients with dexamethasone.