Expression of BDNF and TrKB in Patients With Endometriosis and Their Correlation With Dysmenorrhea

Sha wang, Hua Duan, Bohan Li, Wei Hong, Xiao Li, Yiyi Wang, Zhengchen Guo
In: Research Square · 2021 · doi:10.21203/rs.3.rs-786503/v1 · W3191411274
preprint OA: green CC0
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found higher expression of BDNF and TrKB in endometriosis lesions and eutopic endometrium compared to normal tissue, with increased expression correlating to disease severity and dysmenorrhea.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This preprint investigated expression of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor TrkB in eutopic endometrium and ovarian endometriotic lesions from 46 women undergoing laparoscopic surgery, compared with eutopic/normal endometrium from 16 women with benign ovarian tumors. Using real-time PCR for mRNA and immunohistochemistry for protein, it found higher BDNF and TrkB expression in ovarian endometriotic lesions than in eutopic and normal endometrium, no cyclical change in lesions, higher expression in eutopic versus normal endometrium, and higher levels in stage IV versus earlier stages; dysmenorrhea severity was assessed preoperatively by VAS. The study reported positive correlations between BDNF and TrkB mRNA levels in eutopic endometrium and dysmenorrhea VAS scores, and also correlations between BDNF and TrkB in eutopic and ectopic tissues. The authors note key limitations of a preprint format and, based on the described design, relatively small control and stage subgroup sizes with cross-sectional sampling at surgery. This paper is centrally about endometriosis — it examines BDNF/TrkB expression in endometriotic lesions and relates it to dysmenorrhea severity and disease stage.

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Abstract

Abstract Background: Brain-derived neurotrophic factor (BDNF) has been recognized as a regulator in the formation and maintenance of chronic pain in various chronic disorders. BDNF together with its high-affinity tyrosine kinase type B (TrkB) receptor were found to be extensively expressed in mammalian female reproductive system. However, BDNF and TrkB expression in different stages of endometriosis, and the correlation between their expression in ectopic lesions and endometriosis pain remains unclear. Methods: This study enrolled sixty-two women underwent laparoscopic surgery. Forty-six women diagnosed as ovarian endometrioma, were recruited in the study group. Sixteen women diagnosed as ovarian benign tumors were recruited in the control group. Samples from eutopic endometrium and ovarian endometriotic lesions were obtained at laparoscopic surgery. The message RNA (mRNA) level of BDNF and TrKB was detected by real-time PCR, while the protein level was detected by immunohistochemical staining for eutopic and ectopic endometrium in both groups. Dysmenorrhea was assessed by the visual analogue scale (VAS) before the surgery. Results: The expression of BDNF and TrKB were higher in ovarian endometriotic lesions than those in eutopic endometrium and normal endometrium ( P <0.05), and there was no cyclical change. While their expression in eutopic endometrium were higher than those in the normal endometrium ( P <0.05). The expression of BDNF and TrKB in ovarian endometriotic lesions stage IV were higher than those in stage III and II ( P 0.05). Furthermore, the correlation between the mRNA expression of BDNF, TrKB in eutopic endometrium, and dysmenorrhea VAS score revealed that r=0.52 and 0.56, respectively ( P <0.05). The correlation between BDNF and TrKB in both eutopic and ectopic endometrium were revealed that r=0.82 and 0.66, respectively ( P <0.05). Conclusions: BDNF and TrKB may play essential roles in promoting disease progression during the development of endometriosis, and are closely related to dysmenorrhea caused by endometriosis.

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Outcome instruments

VAS-pain

Condition tags

endometriosisendometriomadysmenorrhea

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (20)

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europepmc
last seen: 2026-06-13T17:25:11.398945+00:00
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License: CC0 · commercial use OK