Abstract
Endometriosis is common in reproductive-age women and its pathology is to increase proliferation and migration to enhance epithelial-to-mesenchymal transition progression (EMT). However, treatments are currently limited, so it is important to explore new therapeutic drugs. Hence, in this study, we investigate the therapeutic effect of fucoidan (FC) on the progression and mechanisms of endometriosis. The cell viability of endometrial cell lines End1/E6E7 and Vk2/E6E7 treated with different concentrations of FC were assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and cell counting. Cell migration was evaluated using wound-healing assay. In an in vivo experiment, female Balb/c mice received surgically induced endometriosis followed by different concentrations of fucoidan for 6 weeks. High-frequency ultrasound imaging was applied to detect subsequent lesion growth. The results demonstrated that fucoidan inhibited the viability and migration ability of End1/E6E7 and Vk2/E6E7 cells. Additionally, the administration of fucoidan reduced the volume and weight of endometriotic lesions, decreased inflammatory cytokines and vascular endothelial growth factor (VEGF) of serum and lesions, and improved EMT proliferation and apoptosis-related protein expression. For the first time, fucoidan indicated anti-proliferative and anti-inflammatory effects as well as inhibited EMT progression and induced apoptosis, improving endometriosis.
Highlights
Endometriosis is a chronic, estrogen-dependent benign inflammatory disease that occurs in reproductive-age women and affects 6–10% of women [1,2]
Since epithelial-to-mesenchymal transition progression (EMT) plays a critical role in endometriosis, which affects proliferation, apoptosis, and migration, we investigated the expression of EMT-related proteins of endometriosis lesions in mice
The pathology of endometriosis is the endometrial-like tissue that migrates to the outside of the uterus, EMT progression shows a critical role in endometriosis [34]
Summary
Endometriosis is a chronic, estrogen-dependent benign inflammatory disease that occurs in reproductive-age women and affects 6–10% of women [1,2]. It presents several severe clinical features, including chronic pelvic pain, dysmenorrhea, dysuria, and infertility [3,4,5]. Biomedicines 2020, 8, 528 endometriosis increases the risk of gynecologic cancers, such as ovarian cancer and breast cancer [6]. The endometriosis pathogenesis has not been cleared, retrograde menstruation has recently become an extensively accepted theory. The factors of endometriosis progression include proliferation, angiogenesis, and epithelial– Endometrial tissue in the menstrual blood flows back through the fallopian tube and into the ovary or peritoneal cavity, thereby adhering to other tissues and growing [7,8,9].
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