ReferenceID 1353
Betulinic Acid Inhibits Endometriosis Through Suppression of Estrogen Receptor β Signaling Pathway
Front Endocrinol (Lausanne)
Endometriosis is an inflammatory gynecological disorder characterized by endometrial tissue growth located outside of the uterine cavity in addition to chronic pelvic pain and infertility. In this study, we aim to develo
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Record Fields
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- Reference Id
- 1353
- Evidence Id
- 17943
- Core Evidence Id
- 17943
- Source Reference Id
- 2708
- Herb2 Reference Id
- HBREF003505
- Subject Paper Key
- HBIN018373_33362719
- Pubmed Id
- 33362719
- Doi
- 10.3389/fendo.2020.604648
- Paper Title
- Betulinic Acid Inhibits Endometriosis Through Suppression of Estrogen Receptor β Signaling Pathway
- Paper Abstract
- Endometriosis is an inflammatory gynecological disorder characterized by endometrial tissue growth located outside of the uterine cavity in addition to chronic pelvic pain and infertility. In this study, we aim to develop a potential therapeutic treatment based on the pathogenesis and mechanism of Endometriosis. Our preliminary data showed that the expression of estrogen receptor beta (ERbeta) was significantly increased, while ERalpha was significantly decreased, in endometriotic cells compared to normal endometrial cells. Further investigation showed that betulinic acid (BA) treatment suppressed ERbeta expression through epigenetic modification on the ERbeta promoter, while had no effect on ERalpha expression. In addition, BA treatment suppresses ERbeta target genes, including superoxide dismutase 2 (SOD2), nuclear respiratory factor-1 (NRF1), cyclooxygenase 2 (COX2), and matrix metalloproteinase-1 (MMP1), subsequently increasing oxidative stress, triggering mitochondrial dysfunction, decreasing elevated proinflammatory cytokines, and eventually suppressing endometriotic cell proliferation, mimicking the effect of ERbeta knockdown. On the other hand, gain of ERbeta by lentivirus infection in normal endometrial cells resulted in increased cell proliferation and proinflammatory cytokine release, while BA treatment diminished this effect through ERbeta suppression with subsequent oxidative stress and apoptosis. Our results indicate that ERbeta may be a major driving force for the development of endometriosis, while BA inhibits Endometriosis through specific suppression of the ERbeta signaling pathway. This study provides a novel therapeutic strategy for endometriosis treatment through BA-mediated ERbeta suppression.
- Journal
- Front Endocrinol (Lausanne)
- Publish Year
- 2020
- Experiment Subject
- Experiment Type
- Cell Experiment
- Phenotype Related
- Inflammatory Gynecological Disorder; Chronic Pelvic Pain; Endometriosis; Infertility; Mitochondrial Dysfunction
- Paper Title Cn
- Paper Title En
- Betulinic Acid Inhibits Endometriosis Through Suppression of Estrogen Receptor β Signaling Pathway
- Bilingual Status
- semi_complete