Protective Effects and Benefits of Olive Oil and Its Extracts on Women's Health.

Women and men share similar diseases; however, women have unique issues, including gynecologic diseases and diseases related to menstruation, menopause, and post menopause. In recent decades, scientists paid more attention to natural products and their derivatives because of their good tolerability and effectiveness in disease prevention and treatment. Olive oil is an essential component in the Mediterranean diet, a diet well known for its protective impact on human well-being. Investigation of the active components in olive oil, such as oleuropein and hydroxytyrosol, showed positive effects in various diseases. Their effects have been clarified in many suggested mechanisms and have shown promising results in animal and human studies, especially in breast cancer, ovarian cancer, postmenopausal osteoporosis, and other disorders. This review summarizes the current evidence of the role of olives and olive polyphenols in women's health issues and their potential implications in the treatment and prevention of health problems in women.

Paeonia lactiflora Enhances the Adhesion of Trophoblast to the Endometrium via Induction of Leukemia Inhibitory Factor Expression.

In the present study, we investigated the role of Paeonia lactiflora Pall. extract on embryo implantation in vitro and in vivo. A polysaccharides depleted-water extract of P. lactiflora (PL-PP) increased LIF expression in human endometrial Ishikawa cells at non-cytotoxic doses. PL-PP significantly increased the adhesion of the human trophectoderm-derived JAr spheroids to endometrial Ishikawa cells. PL-PP-induced LIF expression was decreased in the presence of a p38 kinase inhibitor SB203580 and an MEK/ERK inhibitor U0126. Furthermore, endometrial LIF knockdown by shRNA reduced the expression of integrins ß3 and ß5 and adhesion of JAr spheroids to Ishikawa cells. In vivo administration of PL-PP restored the implantation of mouse blastocysts in a mifepristone-induced implantation failure mice model. Our results demonstrate that PL-PP increases LIF expression via the p38 and MEK/ERK pathways and favors trophoblast adhesion to endometrial cells.

Inhibitory effect of glyceollins on vasculogenesis through suppression of endothelial progenitor cell function.

SCOPE: Endothelial progenitor cells (EPCs) are derived from hematopoietic stem cells, and have the ability to differentiate into mature endothelial cells and contribute to neovascularization. Glyceollins are a type of phytoalexin produced in soybeans under stress conditions. The aim of this study is to determine the effect of glyceollin treatment on EPCs during early tumor vasculogenesis. METHODS AND RESULTS: We found that glyceollin treatment significantly decreased the number of EPC colony-forming units in human cord blood-derived AC133⁺ cells and mouse bone-marrow-derived c-Kit⁺/Sca-1⁺/Lin⁻ cells. Glyceollin treatment diminished the number of lineage-committed EPC cells in a dose-dependent manner (1-20 µM). Glyceollin treatment inhibited EPC migration, tube formation and the mRNA expression of angiopoietin-1 (Ang-1), Tie-2, stromal-derived factor-1 (SDF-1), C-X-C-chemokine receptor-4 (CXCR4), and endothelial nitric oxide synthase (eNOS) in cultured EPCs. Glyceollin treatment suppressed activation of Akt, Erk, and eNOS induced by SDF-1α or vascular endothelial growth factor (VEGF). Treatment with 10 mg/kg glyceollins significantly reduced the number of tumor-induced circulating EPCs and the incorporation of EPCs into neovessels in bone marrow transplanted mice. CONCLUSION: These results suggest that glyceollins inhibit the function of EPCs in tumor neovascularization. Glyceollins from soybean elicitation could be beneficial in prevention of cancer development via vasculogenesis.

Ginsenoside Rg3 inhibits endothelial progenitor cell differentiation through attenuation of VEGF-dependent Akt/eNOS signaling.

Endothelial progenitor cells (EPCs) play a critical role both in vascular repair after cell transplantation for ischemic diseases and in the growth of early tumors by intervening with the angiogenic switch during tumor progression. This paper reports on the effect of ginsenoside Rg3 in EPCs as a candidate angiogenesis inhibitor for in vitro functional assays. CD34⁺ cells were isolated from human cord blood and the study investigated whether or not ginsenoside Rg3 regulated EPC bioactivities including cell proliferation, differentiation, migration and tube formation. Although ginsenoside Rg3 did not affect the ex vivo expansion of CD34 and/or KDR (VEGFR2) stem/progenitor cells, treatment with ginsenoside Rg3 led to a significant decrease in CD34-expressing cells, specifically the absolute number of expanded CD34⁺ cells. Importantly, a significantly decreased number of EPC colony-forming units among human cord blood-derived CD34⁺ cells was observed, implying that ginsenoside Rg3 inhibited EPC differentiation, in particular, the commitment to primitive EPC colonies (the early stage of EPC differentiation). Moreover, treatment of CD34-derived EPCs with ginsenoside Rg3 resulted in the attenuation of VEGF-dependent Akt/eNOS signaling as well as the inhibition of migration and tube formation. In conclusion, this study provides in vitro evidence for ginsenoside Rg3 as a potential therapeutic molecule, specifically as an angiogenesis inhibitor that functions by attenuating EPC bioactivities.