Purpose: To investigate the effect of atractylenolide on recurrent spontaneous abortion (RSA).Methods: The HTR-8/SVneo was established as an in vitro cell model of RSA. Cell viability and proliferation were determined using CCK8 and BrdU staining, while cell migration and invasion were determined by cell scratch and transwell assays.Results: Atractylenolide significantly increased cell viability, and enhanced the number of BrdU-positive cells of HTR-8/SVneo (p < 0.01). Atractylenolide also significantly promoted cell migration and invasion (p < 0.01), and increased protein expression of MMP-9, MMP-2, and N-cadherin, but reduced Ecadherin. Atractylenolide also increased the phosphorylation of ERK (p < 0.01).Conclusion: Atractylenolide enhances cell proliferation and migration of HTR-8/SVneo through activation of ERK signaling. Further studies using animal models are recommended to determine the protective role of atractylenolide against RSA, in vivo.

Deficiency of decidual NK (dNK) cell number and function has been widely regarded as an important cause of spontaneous abortion. However, the metabolic mechanism underlying the crosstalk between dNK cells and embryonic trophoblasts during early pregnancy remains largely unknown. Here, we observed that enriched glutamine and activated glutaminolysis in dNK cells contribute to trophoblast invasion and embryo growth by insulin-like growth factor-1 (IGF-1) and growth differentiation factor-15 (GDF-15) secretion. Mechanistically, these processes are dependent on the downregulation of EGLN1-HIF-1α mediated by α-ketoglutarate (α-KG). Blocking glutaminolysis with the GLS inhibitor BPTES or the glutamate dehydrogenase inhibitor EGCG leads to early embryo implantation failure, spontaneous abortion and/or fetal growth restriction in pregnant mice with impaired trophoblast invasion. Additionally, α-KG supplementation significantly alleviated pregnancy loss mediated by defective glutaminolysis in vivo, suggesting that inactivated glutamine/α-ketoglutarate metabolism in dNK cells impaired trophoblast invasion and induced pregnancy loss.

Background This study sought to compare the surgical results of patients undergoing a laparoendoscopic single-site myomectomy (LESS-M) and a conventional laparoscopic myomectomy (CLM) at our hospital. Methods The basic data of 233 patients undergoing LESS-M and 233 patients undergoing CLM at the Obstetrics and Gynecology Hospital Affiliated to Fudan University were collected from January 2018 to January 2020, and the results of the operations were compared by evaluating a number of factors, including operation time, intraoperative bleeding, postoperative fever, and postoperative maximum body temperature. Results The operation times of the LESS-M and CLM groups were 83.9±33.4 and 75.2±26.7 min, respectively; the difference between the groups was statistically significant. The surgical blood loss of the LESS-M group was 86.1±76.9 mL, and that of the CLM group was 83.8±79.9 mL (P>0.05). When the diameter of a fibroid was ≥8 cm, a fibroid was located in the posterior wall or the number of fibroids was ≥4, the operation time of the CLM group was shorter than that of the LESS-M group. When the diameter of a fibroid was ≥8 cm, the blood loss of the CLM group was less than that of the LESS-M group. Conclusions LESS-M is safe and feasible. If the diameter of a fibroid is ≥8 cm, the fibroid is located in the posterior wall, or the number of fibroids is ≥4, the utility of single-port surgery should be carefully considered.

Endometrium is the mucosal lining of the uterus which expressed a cyclic process of proliferation, secretion and scaling under the control of hormones secreted by the ovary, and it also plays an indispensable role in the embryo implantation, the constitution of fetal-maternal interface, and the maintaining of pregnancy. In pathophysiological conditions, the abnormality or disorder of endometrium may lead to endometrium-related diseases, such as endometriosis, endometrium hyperplasia and even endometrial carcinoma. In recent years, more and more evidence revealed that autophagy exists in both the endometrium stroma cells and epithelial cells, and the activity of autophagy is changed in the different phases of menstruation, as well as in the endometrium-related diseases. Here, we aim to review the activity level, the regulatory factors and the function of autophagy in physiological and pathophysiological endometria, and to discuss the potential value of autophagy as a target for therapies of endometrium-related diseases.

Objective: To investigate whether kynurenine/aryl hydrocarbon receptor (AHR) affects the maternal-fetal tolerance by involving the differentiation of T helper 17 (Th17)/regulatory T (Treg) cells, and to provide theoretical basic for new treatment of unexplained abortion. Methods: Flow cytometry (FCM) was used to detect the expression of AHR in peripheral/decidual CD4(+) T, Treg, and Th17 cells. The effect of Kyn on the differentiation of peripheral/decidual nave T-cells under Treg-/Th17-polarizing condition was detected by FCM; enzyme-linked immunosorbent assay was performed to examine the level of Kyn in villus and decidual tissues from normal pregnancy (NP) and unexplained abortion (UA). Student's t-test in the case of two groups or one-way ANOVA in multiple groups was used. Results: AHR expression in CD4(+) T-cells was decreased in decidua versus blood in early pregnancy (P < 0.0001). Kyn could promote the differentiation of peripheral and decidual nave T-cells to Th17 cells under Treg-polarizing conditions (P < 0.01). There was no statistical significance about the concentration of Kyn in decidual or villi tissues between NP and UA, and compared with NP, the expression of AHR in decidual CD4(+) T-cells from UA was increased (P < 0.001). Conclusions: Kyn/AHR promotes Th17 and restricts Treg cells' differentiation, which is involved in maintaining the balance of Treg/Th17 cells at the maternalufetal interface.

Recurrent spontaneous abortion (RSA) is a common health problem that affects about 5% of fertile women, when it occurs for unknown reasons, it is called unexplained recurrent spontaneous abortion (URSA). Traditional Chinese medicine, such as Bu-Shen-Yi-Qi formula which consists of Dangshen, Tusizi, Baizhu, Baishuo, Duzhong, Sangjisheng, Sugeng, and Tiaohuangqin, has played an invaluable role in the treatment of RSA since ancient times. However, the mechanism of how it takes effect is still not clear. To identify Bu-Shen-Yi-Qi formula could modulate immune condition at maternal-fetal interface via its effect on trophoblasts, HTR-8 of different treatment were co-cultured with peripheral or decidual natural killer (NK) cells, and the receptors such as NKP30 and NKP46 expression on NK cells were measured by flow cytometry (FCM). In this study, we found that herb medium could increase the IDO expression at appropriate concentrations. As an inhibitor of IDO, 1-MT could impair the inhibitory function of trophoblasts on NK cells. Furthermore, Bu-Shen-Yi-Qi formula could enhance the inhibitory function of trophoblasts on NK cells. In conclusion, Bu-Shen-Yi-Qi formula can inhibit NK cytotoxicity by up-regulating IDO expression in trophoblasts and play a role in the treatment of URSA patients.