Adiponectin Reduces Embryonic Loss Rate and Ameliorates Trophoblast Apoptosis in Early Pregnancy of Mice with Polycystic
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ORIGINAL ARTICLE
Adiponectin Reduces Embryonic Loss Rate and Ameliorates Trophoblast Apoptosis in Early Pregnancy of Mice with Polycystic Ovary Syndrome by Affecting the AMPK/PI3K/Akt/FoxO3a Signaling Pathway Wenqian Zhang 1 & Meng Zuo 1 & Juan Lu 1 & Yuxia Wang 1 Received: 3 December 2019 / Revised: 26 May 2020 / Accepted: 8 June 2020 # The Author(s) 2020
Abstract Reports in recent years have suggested that adiponectin (APN) improves insulin resistance and inhibits apoptosis by activating the AMP-activated protein kinase (AMPK) pathway and the PI3K/Akt signaling pathway after binding to its receptor. This study aims to explore the mechanism by which APN reduces embryo loss rate and trophoblast apoptosis in early pregnancy of mice with polycystic ovary syndrome (PCOS). PCOS mice were subcutaneously injected with APN (10 μg mg kg−1 day−1) on 11 consecutive days from the 3rd day of pregnancy onwards to observe the change of the embryo loss rate of PCOS mice induced by APN. Quantitative real-time PCR and Western blot were used to determine the relative expressions of mRNA and the proteins AMPK, PI3K, and Akt in mouse uterine tissue. At the same time, primary cultured mouse villous trophoblast cells were used to further explore the underlying mechanisms in vitro. APN significantly reduces the pregnancy loss rate of PCOS mice. At the same time, APN increases phosphorylation and mRNA expression levels of AMPK, PI3K, and Akt in PCOS mouse uterine tissue. In addition, trophoblast cells of model mice were treated with APN and inhibitors, and APN was found to reduce trophoblast cell apoptosis by affecting the phosphorylation levels of AMPK, PI3K, Akt, and FoxO3a proteins. APN reduces the embryo loss rate and ameliorates trophoblast apoptosis in PCOS mice by affecting the AMPK/PI3K/AKT/FoxO3a signaling pathway. Keywords Polycystic ovarian syndrome . Adiponectin . Trophoblast cells . AMPK . PI3K . AKT
Introduction Polycystic ovarian syndrome (PCOS) is one of the most common endocrine and metabolic disorders in women of childbearing age. PCOS has an average incidence of 6–20% [1, 2], and obesity may establish a crucial barrier for effective fertility treatment in females who have PCOS. Obese women with PCOS had a lower rate of clinical pregnancy and a higher rate of abortions [3]. The etiology of PCOS is not yet fully understood. As researchers around the world gain a better understanding of PCOS,
* Yuxia Wang [email protected] 1
Department of Reproductive Medicine, The First Affiliated Hospital, Jinan University, 601 West Huangpu Avenue, Guangzhou 510000, Guangdong, People’s Republic Of China
the awareness of the multisystem characteristics of this disease is increasing [4, 5].The syndrome can cause a range of health problems, including hyperandrogenemia (HA), insulin resistance (IR), ovulatory dysfunction, infertility, miscarriage, hyperlipidemia, cardiovascular disease, endometrial dysfunction, and obesity [6]. Therefore, PCOS is no longer simply considered an ovarian disease [7]. APN has anti-inflammatory, antioxidan
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