Apigenin suppressed tumor necrosis factor α-induced cell proliferation and prostaglandin E2 expression via the attenuation of nuclear factor κB pathway in endometriotic stromal cells in vitro. Apigenin reduced the mitogenic activity and inflammatory reaction in endometriotic stromal cells.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.fertnstert.2010.09.046 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Silencing of FZD7 Inhibits Endometriotic Cell Viability, Migration, and Angiogenesis by Promoting Ferroptosis.
Cell Biochem Biophys
January 2025
Department of Obstetrics and Gynecology, Lishui Municipal Central Hospital, Lishui, Zhejiang, 323000, China.
Background: Endometriosis (EMS) is a difficult gynecological disease to cure. Frizzled-7 (FZD7) has been shown to be associated with the development of EMS, but its specific mechanism remains unclarified. This study aims to explore the role of FZD7 in EMS.
View Article and Find Full Text PDFSingle-cell and spatial transcriptomic profiling revealed niche interactions sustaining growth of endometriotic lesions.
Cell Genom
January 2025
National Clinical Research Center for Obstetric & Gynecologic Diseases, Department of Obstetrics and Gynecology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China. Electronic address:
Endometriosis is a chronic condition with limited therapeutic options. The molecular aberrations promoting ectopic attachment and interactions with the local microenvironment sustaining lesion growth have been unclear, prohibiting development of targeted therapies. Here, we performed single-cell and spatial transcriptomic profiling of ectopic lesions and eutopic endometrium in endometriosis.
View Article and Find Full Text PDFALKBH5 promotes autophagy and progression by mediating m6A methylation of lncRNA UBOX5-AS1 in endometriosis.
Am J Physiol Cell Physiol
January 2025
Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Long noncoding RNA (lncRNA) and N6-methyladenosine (m6A) methylation modification have recently been suggested as potential functional modulators in ovarian endometriosis, however, the function and mechanism of m6A-modified lncRNA in ovarian endometriosis remain poorly understood. In this study, we demonstrated that lncRNA UBOX5-AS1 expression was significantly elevated in ovarian endometriosis tissue and primary ectopic endometrial stromal cells. The expression of lncRNA UBOX5-AS1, which has m6A modifications, was highly positively correlated with demethylase Alk B homologous protein 5 (ALKBH5) expression and autophagy.
View Article and Find Full Text PDFThe PKM2/HIF-1α Axis is Involved in the Pathogenesis of Endometriosis via TGF-β1 under Endometrial Polyps.
Front Biosci (Landmark Ed)
December 2024
Department of Reproductive Medicine, Dongying People's Hospital, 257091 Dongying, Shandong, China.
Background: Endometriosis patients exhibit a cancer-like glycolytic phenotype. The pyruvate kinase M2 (PKM2)/hypoxia-inducible factor-1 alpha (HIF-1α) axis plays important roles in glycolysis-related diseases, but its role in patients with endometrial polyps (EPs) combined with endometriosis has not been validated.
Methods: EP samples were collected from patients with and without endometriosis.
Macranthoidin B restrains the epithelial-mesenchymal transition through COX-2/PGE pathway in endometriosis.
Front Pharmacol
December 2024
School of Chinese Materia Medica, Chongqing University of Chinese Medicine, Chongqing, China.
Introduction: Macranthoidin B is one of the primary and unique triterpenoid saponin metabolites from Hand. -Mazz, which is used to treat endometriosis (EMS) in traditional Chinese medicine. However, the effect of macranthoidin B remains unknown in EMS.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!