By immunohistochemistry the GR protein was localized to the nuclei of cervical stroma, squamous epithelium, vascular endothelium and glandular epithelium in samples from the NP, TP and PP groups. By image analysis the GR degrees were
Identified in SQ and stroma. The stromal cells contain vascular epithelium and the leukocytes within the stroma. Body cells within vessels are excluded from the image analysis. Strong immunostaining was contained in SQ, specially in the
basal and parabasal cell layers. There clearly was an important decrease in immunostaining of the PP group when compared with the TP group, equally in stroma and SQ. The stromal GR immunostaining was increased in the TP group in comparison with the NP
and PP teams. It absolutely was noted in all organizations that GE, vascular endothelium and some perivascular and intravascular leukocytes stained optimistic for GR, while some leukocytes were bad. NO stimulates PGE2 release from human cervical
tissue explants, and is just a effective regulator of COX 2 thus increasing local PGE2 concentrations in inflammatory cells. NO donors do induce cervical ripening in human pregnancy in the very first trimester, at expression and in non expectant mothers.
Besides, treatment with the NO donor isosorbide 5 mononitrate stimulates production of e. g. COX 2 and PGE2 in human cervix. The activity of NO on cervical ripening is apparently achieved by effects on connective tissue and smooth
muscle cells in the same way as previously been proven for prostaglandins. Our hypothesis is that glucocorticoids exert a direct receptor mediated effect in the human cervix uteri, and that a changed biological response to glucocorticoids
could be a process behind the activities causing cervical ripening at parturition. Because NFB has compared functions in inflammatory reactions as compared to GR, we presume that NFB could also be a of the inflammatory events
Ultimately causing cervical ripening. These inflammatory activities might be mediated via factors such as the PAF R, iNOS and/or COX enzymes.