Recurrent spontaneous abortion (RSA), defined as the loss of ≥2 consecutive pregnancies before the 24th gestational week, affects 1%-2% women during their reproductive age [1]. As a common condition in reproductive medicine, RSA is reported in 1-2% of fertile couples seeking pregnancy and inflicts a significant physical, emotional, and financial burden on many families [2]. Many factors are thought to contribute to RSA, such as parental chromosomal abnormalities, maternal thrombophilia, immune dysfunction, and various endocrine disorders [3]. In addition, the age of the pregnant mother has also been reported to be a strong independent risk factor for miscarriage, and in particular, the risk of fetal miscarriage greatly increases after 35 years of age [4]. However, in many cases, the causes of RSA could not be easily identified, while the evidence-based diagnostic and treatment strategies are in short supply and the prospects of treatment are not as promising as they could be [5].Interleukin 23 (IL-23), which is composed of a p40 subunit and a specific p19 subunit, belongs to the IL-12 cytokine family and is secreted by dendritic cells and macrophages [6,7]. Accumulated reports have confirmed that IL-23 participates in the development of some autoimmune inflammatory diseases, including psoriasis, arthritis, and inflammatory bowel disease, thus serving as a critical therapeutic target for the improvement of inflammatory diseases [8][9][10]. In addition, another study reported that IL-23 was upregulated in patients with RSA [11]. Moreover, both IL-17 and IL-23 were verified to inhibit Langerhans cell (LC) migration in a psoriasis As a vital problem in reproductive health, recurrent spontaneous abortion (RSA) affects about 1% of women. We performed this study with an aim to explore the molecular mechanism of interleukin-23 (IL-23) and find optimal or effective methods to improve RSA. First, ELISA was applied to evaluate the expressions of IL-23 and its receptor in HTR-8/SVneo cells after IL-23 treatment. CCK-8, TUNEL, wound healing and transwell assays were employed to assess the proliferation, apoptosis, migration and invasion of HTR-8/SVneo cells, respectively. Additionally, the expressions of apoptosis-, migration-, epithelial-mesenchymal transition-(EMT-) and p38 MAPK signaling pathway-related proteins were measured by western blotting. To further investigate the relationship between IL-23 and p38 MAPK signaling pathway, HTR-8/SVneo cells were treated for 1 h with p38 MAPK inhibitor SB239063, followed by a series of cellular experiments on proliferation, apoptosis, migration and invasion, as aforementioned. The results showed that IL-23 and its receptors were greatly elevated in IL-23-treated HTR-8/SVneo cells. Additionally, IL-23 demonstrated suppressive effects on the proliferation, apoptosis, migration, invasion and EMT of IL-23-treated HTR-8/SVneo cells. More importantly, the molecular mechanism of IL-23 was revealed in this study; that is to say, IL-23 inhibited the proliferation, apoptosis, migration, invas...