Endometriosis (EMS) is a common gynecological disease. Prostaglandin E2 (PGE2), which induces chronic pelvic inflammation and cell pyroptosis, a form of programmed cell death based on inflammasome activation, are involved in EMS, but the extent of their involvement and roles remain unclear. The present study aimed to evaluate PGE2-induced pyroptosis in EMS and the influence of PGE2 in EMS progression. Using western blotting, it was found that the expressions of PGE2 and pyroptosis-related proteins (NLRP3, cleaved caspase-1, interleukin (IL)-1β and IL-18) were higher in EMS tissues than in normal endometrial tissues. The levels of PGE2, IL-1β, and IL-18 in the serum of patients with EMS and cell culture fluids were also detected. Using the transwell assay, we verified that PGE2 promoted hEM15A migration via the NLRP3/caspase-1 pyroptotic pathway, and PGE2-induced pyroptosis upregulated the expressions of high mobility group box 1 (HMGB1), E-cadherin, and vimentin. Immunohistochemistry analysis confirmed that PGE2-induced pyroptosis contributed to EMS invasion. These results suggest that PGE2-induced pyroptosis affects the progression of EMS by changing the migration ability of pyroptotic cells and upregulating the expression of HMGB1, E-cadherin, and vimentin. Our findings provide crucial evidence for new treatment pathways and use of anti-inflammatory drugs in EMS.

The objective of this systematic review is to synthesize the available evidence on the effectiveness of magnesium supplements on the markers of inflammation, oxidative stress (OS), and metabolism in PCOS patients and to provide a basis for its clinical treatment. Electronic databases (PubMed, Cochrane Library databases, Embase, Web of science, CMB, CNKI, VIP, Wan Fang and ClinicalTrials.gov) were searched from their inception until January 2022. Randomized controlled trials (RCTs) for PCOS undergoing therapy with magnesium supplementation alone or in combination with other agents. The primary outcomes were the markers of blood glucose and OS.363 patients from nine RCTs were included in the current systematic review. Four of the nine studies reported the effects of magnesium supplementation alone on OS or metabolic markers in women with PCOS. Whilemagnesium supplementation alone did not show any significant improvement in the markers of inflammation, OS or metabolism in PCOS, seven of the nine articles reported the effect of magnesium co-supplementation on OS or metabolic markers in PCOS patients. Magnesium combined with vitamin E or zinc-calcium-vitamin D significantly improved glucose and lipid metabolism in PCOS patients. Magnesium intake alone did not lead to a significant improvement in the markers of OS, blood glucose, or serum lipids in PCOS. However, magnesium combined with other supplements (vitamin E, zinc, zinc-calcium-vitamin D) significantly improved serum hs-CRP, insulin, HOMA-IR, TG, TC levels, and the improvement in OS markers was inconclusive. The effect of magnesium and melatonin supplementation on the markers of metabolism needs to be further verified.System Review Registration: PROSPERO https://www.crd.york.ac.uk/PROSPERO/#myprospero, CRD42022303410.

With the continuous advances in molecular biotechnology, many new cell death methods have been discovered. Pyroptosis is a programmed cell death process that differs from apoptosis and autophagy in cell morphology and function. Compared with apoptosis and autophagy, pyroptosis is primarily mediated by intracellular inflammasome and gasdermin D of the gasdermin protein family and involves the release of numerous inflammatory factors. Pyroptosis has been found to be involved in the occurrence and development of infectious diseases and other diseases involving the nervous system and the cardiovascular system. Recent studies have also reported the occurrence of pyroptosis in tumor cells. Accordingly, exploring its effect on tumors has become one of the research hotspots. Herein, recent research progress on pyroptosis is reviewed, especially its role in the development of gynecological tumors. As the pathogenesis of gynecological tumor is better understood, new targets have been introduced for the prevention and clinical treatment of gynecological tumors.

Endometriosis (EMS) is a chronic disease that can cause dysmenorrhea, chronic pelvic pain, and infertility, among other symptoms. EMS diagnosis is often delayed compared to other chronic diseases, and there are currently no accurate, easily accessible, and non-invasive diagnostic tools. Therefore, it is important to elucidate the mechanism of EMS and explore potential biomarkers and diagnostic tools for its accurate diagnosis and treatment. In the present study, we comprehensively analyzed the differential expression, immune infiltration, and interactions of EMS-related genes in three Homo sapiens datasets. Our results identified 332 differentially expressed genes (DEGs) associated with EMS. Gene ontology analysis showed that these changes mainly focused on the positive regulation of endometrial cell proliferation, cell metabolism, and extracellular space, and EMS involved the integrin, complement activation, folic acid metabolism, interleukin, and lipid signaling pathways. The LASSO regression model was established using immune DEGs with an area under the curve of 0.783 for the internal dataset and 0.656 for the external dataset. Five genes with diagnostic value, ACKR1, LMNB1, MFAP4, NMU, and SEMA3C, were screened from M1 and M2 macrophages, activated mast cells, neutrophils, natural killer cells, follicular T helper cells, CD8⁺, and CD4⁺ cells. A protein−protein interaction network based on the immune DEGs was constructed, and ten hub genes with the highest scores were identified. Our results may provide a framework for the development of pathological molecular networks in EMS.