Association between ACE1 and missed abortion: ACE1 promotes H2O2-induced trophoblast cell injury in vitro†.

The aim of this study was to evaluate the role of angiotensin-converting enzyme 1 (ACE1) in H2O2-induced trophoblast cell injury and the potential molecular mechanisms. Oxidative stress was modeled by exposing HTR-8/SVneo cells to 200 µM H2O2. Western blot and real-time quantitative PCR methods were used to detect protein and mRNA expression level of ACE1 in chorionic villus tissue and trophoblast HTR-8/SVneo cell. Inhibition of ACE1 expression was achieved by transfection with small interfering RNA. Then flow cytometry, Cell Counting Kit-8, and Transwell assay was used to assess apoptosis, viability, and migration ability of the cells. Reactive oxygen species (ROS) were detected by fluorescent probes, and malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) activities were determined by corresponding detection kits. Angiotensin-converting enzyme 1 expression was upregulated in chorionic villus tissue of patients with missed abortion (MA) compared with individuals with normal early pregnancy abortion. H2O2 induced elevated ACE1 expression in HTR-8/SVneo cells, promoted apoptosis, and inhibited cell viability and migration. Knockdown of ACE1 expression inhibited H2O2-induced effects to enhance cell viability and migration and suppress apoptosis. Additionally, H2O2 stimulation caused increased levels of ROS and MDA and decreased SOD and GSH activity in the cells, whereas knockdown of ACE1 expression led to opposite changes of these oxidative stress indicators. Moreover, knockdown of ACE1 attenuated the inhibitory effect of H2O2 on the Nrf2/HO-1 pathway. Angiotensin-converting enzyme 1 was associated with MA, and it promoted H2O2-induced injury of trophoblast cells through inhibiting the Nrf2 pathway. Therefore, ACE1 may serve as a potential therapeutic target for MA.

Exploratory study on the mechanism of necrotic effect of nourishing cells in the context of genital tract infection in premature rupture of membranes.

To explore the mechanism of necrotic effect of nourishing cells in the context of genital tract infection in premature rupture of membranes (PROM). One hundred eight patients with PROM treated at our hospital from June 2020 to June 2022 were selected as the PROM group. Simultaneously, 108 cases of normal full-term pregnant women were chosen as the control group. Western blot analysis was performed to measure the relative expression levels of cysteinyl aspartate specific proteinase-1 (Caspase-1), cysteinyl aspartate specific proteinase-3 (Caspase-3), nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3), and interleukin (IL)-1ß proteins, which are associated with necrosis of placental nourishing cells, in the placenta of both groups. TUNEL staining was used to detect the number of apoptotic placental nourishing cells. The differences in necrotic factors of placental nourishing cells were analyzed between full-term and preterm cases in the PROM group, as well as among patients with different genital tract infections. The apoptotic count of placental nourishing cells in the PROM group was 58.46 ±â€…11.26 cells/field, which was markedly higher than that of the control group (P < .05). The relative expression levels of the necrotic factors Caspase-1, Caspase-3, NLRP3, and IL-1ß proteins in placental nourishing cells of the PROM group were 1.32 ±â€…0.26, 1.19 ±â€…0.30, 1.29 ±â€…0.28, and 1.23 ±â€…0.24, respectively. These values were significantly higher than those of the control group (P < .05). The relative expression levels of the necrotic factors Caspase-1, Caspase-3, NLRP3, and IL-1ß proteins in placental nourishing cells were compared between full-term and preterm patients in the PROM group (P > .05). The relative expression levels of the necrotic factors Caspase-1, Caspase-3, NLRP3, and IL-1ß proteins in placental nourishing cells were higher in patients with multiple genital tract infections compared to those with single infections or no infections in the PROM group (P < .05). PROM is associated with a significant upregulation of placental nourishing cell apoptosis and necrotic factors, including Caspase-1, Caspase-3, NLRP3, and IL-1ß proteins. This upregulation is correlated with the presence of genital tract infections.

Role of menopausal hormone therapy in the prevention of postmenopausal osteoporosis.

The use of menopausal hormone therapy (MHT) has declined due to concerns about its potential side effects. However, its pivotal role in managing postmenopausal osteoporosis is gaining increased recognition. In this article, we explore how MHT assists postmenopausal women in maintaining bone health and preventing fractures. Recent research indicates that MHT significantly reduces the risk of fractures in women. This benefit is evident regardless of a woman's bone mineral density or their use of progestogens. However, there is limited evidence suggesting that the skeletal benefits continue once the treatment is discontinued. Possible complications of MHT include heart attacks, clots, strokes, dementia, and breast cancer. The most suitable candidates for MHT are women who have recently entered menopause, are experiencing menopausal symptoms, and are below 60 years of age with a minimal baseline risk of adverse events. The treatment is available to those who meet these criteria. For women undergoing premature menopause, MHT can be considered as a means to protect bone health, especially if initiated before menopause or if accelerated bone loss is documented soon after menopause. Such decisions should be made after evaluating individual risk factors and benefits.