The aspirin treated and non-treated high risk groups, an overall advantageous
The aspirin treated and non-treated high risk groups, an overall advantageous effect of aspirin preventing OHSS might be seen. We strongly advise, therefore, the use of low-dose aspirin to prevent OHSS or to reduce its severity in all cases associated with high risk of that severe complication of ovulation induction. The coordinated interplay between platelets and ovaries may be accomplished further by the brain-derived neurotrophic factor (BDNF) – Sigma-1 receptor ?Akt ?eNOSsystem. Down-regulation of the system has been proved to be a pathogenetic factor for depression, cardiovascular diseases, diabetes mellitus type 2 and for several components of metabolic syndrome. The activation of S ma-1R signaling has emerged as a link between these pathologies [36,37]. BDNF is mainly produced by the brain accounting for over 70 in the circulation. Additional BDNF sources are the vascular endothelium, smooth muscle cells and activated monocytes/lymphocytes. It readily crosses the blood rain barrier, circulates in the plasma and is taken up and stored in the platelets. Upon platelet activation/ clotting BDNF is released to the extracellular fluid and platelet derived serum BDNF closely correlates with that in the brain [38,39]. Importantly, positive correlation has been documented between BDNF and serotonin release [40,41]. BDNF and serotonin are assumed to act synergistically as serotonin secretion, turnover and signaling is regulated by BDNF, while serotonin in turn controls BDNF production [41]. BDNF and its receptors are widely Quinagolide (hydrochloride) site distributed in peripheral tissues and implicated in modulating ovarium function and diseases related to ovarium dysfunction. With this contention in line Sigma-1R stimulation with selective serotonin reuptake inhibitors (SSRI) in ovariectomized animals and in postmenopausal women improved depressive disorders and provided cardiovascular protection [42]. This beneficial effect of SSRI is achieved by increased conversion of the precursor proBDNF to mature BDNF and its enhanced secretion into the extracellular space [43]. Stimulation of Sigma-1R by ovarial steroids, dehydroepiandrosterone (DHEA) or pregnelolone (PREG) and/or by their sulfates (DHEAS, PREGS) resulted in similar protection in experimental or clinical settings [44]. Interestingly, there are marked cyclic variations in platelet BDNF levels during menstruation. In the second half of menstrual cycle endometrial cells produce substantial amount of BDNF which is taken up by the platelets. The reduced accumulation of endometrium-derived BDNF in the platelets may lead to clinical consequences as seen in menopausa [45]. In a most recent comprehensive review detailed analysis is presented on the importance of BDNF in the paracrine regulation of ovarian function [46]. BDNF has been PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27766426 shown to stimulate the early and final stage of folliculogenesis, oocyte maturation and early embryonic development. In women undergoing IVF treatment it was present PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27385778 in the follicular fluid, and cumulus and granulosa cells were identified as its major source. Significant positive correlation was found between circulating estradiol and BDNF levels and its ovarian secretion could be enhanced with LH, FSH and hCG administration. It is to be noted that BDNF release by the platelets was notB is et al. Journal of Ovarian Research 2014, 7:55 http://www.ovarianresearch.com/content/7/1/Page 5 ofmentioned in this particular review, however accumulating evidences suggest that platelet-derived mediator.
