Abstract

BackgroundBrain-derived neurotrophic factor (BDNF) is a known regulator of the development and maintenance of chronic pain in various chronic disorders. Together with its high-affinity tyrosine kinase type B (TrKB) receptor, BDNF is extensively expressed in the mammalian female reproductive system. However, BDNF and TrKB expression in different stages of endometriosis and the relationship between the expression of each in ectopic lesions and endometriosis pain remain unclear.MethodsSixty-two women who underwent laparoscopic surgery were enrolled in this study: forty-six diagnosed with ovarian endometrioma (study group) and sixteen diagnosed with ovarian benign tumours (control group). Samples from eutopic endometrium and ovarian endometriotic lesions were obtained at laparoscopic surgery. BDNF and TrKB messenger RNA (mRNA) and proteins levels in the eutopic and ectopic endometrium of both groups were measured by real-time PCR and immunohistochemical staining, respectively. Before the surgery the visual analogue scale (VAS) was used to measure dysmenorrhoea.ResultsBDNF and TrKB expression levels were higher in ovarian endometriotic lesions than in eutopic endometrium and normal endometrium (P < 0.05), and there was no cyclical change. Furthermore, their expression levels were higher in eutopic endometrium than in normal endometrium (P < 0.05), and BDNF and TrKB levels were higher in stage IV ovarian endometriotic lesions than in stage II and III lesions (P < 0.05), with their expression being non-significantly higher in stage III than in stage II (P > 0.05). Additionally, correlation coefficients for the association analysis between the mRNA expression of BDNF or TrKB in eutopic endometrium and the dysmenorrhoea VAS score were r = 0.52 and r = 0.56 for BDNF and TrKB, respectively (P < 0.05). The correlation coefficients for the associations between BDNF and TrKB in both the eutopic and ectopic endometrium were r = 0.82 and r = 0.66, respectively (P < 0.05).ConclusionsBDNF and TrKB are closely related to dysmenorrhoea caused by endometriosis and may be important in the pathobiology or pathophysiology of endometriosis.

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