BACKGROUND
The predominant symptom in endometriosis is pain. Now known is the role of VIP, VIPR1, iNOS, COX2 in inflammation and regulation of the immune response, as well as vasoconstriction and vasodilatation of blood vessels. However, the participation of these proteins in the induction of pain associated with the ratio of vasoconstriction and vasodilatation of microvessels in endometriosis has not been established.
OBJECTIVE
To evaluate the role of VIP, VIPR1, iNOS, COX2 in vasoconstriction and vasodilatation of endometrial vessels in endometriosis for the induction of pain.
METHOD
Enzyme-linked immunosorbent assay was used to determine the content of VIP, VIPR1, iNOS, COX2 in the peritoneal fluid and in the blood; immunohistochemistry was used to evaluate the expression of VIP, VIPR1, iNOS, COX2 in vessels; western blotting was used to evaluate protein expression of VIP, VIPR1, iNOS, COX2; the polymerase chain reaction was used to evaluate the expression of VIP mRNA, VIPR1 mRNA, iNOS mRNA, COX2 mRNA in eutopic and ectopic endometrium in patients with endometriosis and pelvic pain.
RESULTS
In a comparative analysis of the content of VIP, VIPR1, NOS, COX2 in the peritoneal fluid and in the blood according to enzyme-linked immunosorbent assay (ELISA); expression in vessels according to immunohistochemical analysis (IHC), protein expression according to Western blotting (WB), expression of mRNA according to polymerase chain reaction (RT-qPCR) in eutopic and ectopic endometrium in patients with endometriosis and pelvic pain was statistically shown a significant increase in the studied parameters in the group of patients with endometriosis and pelvic pain.
CONCLUSION
At the proteomic and transcriptomic levels, the role of vasoactive intestinal peptide (VIP) in the implementation of microenvironment inflammation together with VIPR1, iNOS, COX2 has been proved. Accumulation in microvessels of VIP, VPAC1, iNOS, COX2 leads to excessive vasodilatation due to VIP, VPAC1, iNOS with simultaneous vasoconstriction of microvessels due to COX2 and generated prostaglandins. Identified changes contribute to the implementation of pain with endometriosis. The mismatch between vasodilatation and vasoconstriction of the endometrial microvessels in endometriosis can be used to assess pain and choose treatment tactics.