Involvement of bradykinin and bradykinin B1 receptor in patients with endometriosis

Xin Meng, Ying Li, Qingxue Li, Jian Yang, Mingli An, Xinping Fu, Shuancheng Zhang, Jingwei Chen
Experimental and therapeutic medicine · 2021 · vol. 22(5) , pp. 1240 · doi:10.3892/etm.2021.10675 · PMID:34539836 · W3198370897
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found that bradykinin and its B1 receptor are elevated in endometriosis patients and correlate with pain intensity, suggesting their involvement in endometriosis-associated pain pathogenesis.

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

This study examined whether bradykinin (BK), its B1 receptor (BKB1R), and related prostaglandins contribute to endometriosis-associated pain by measuring serum BK, prostaglandin E2 (PGE2), and prostaglandin F2α (PGF2α), and assessing BKB1R protein/mRNA expression in eutopic and ectopic endometrial tissues from 50 women with endometriosis versus 20 surgical controls. Compared with controls, the endometriosis group showed increased BKB1R protein and mRNA expression and elevated circulating BK, PGE2, and PGF2α, with strong correlations among PGE2, PGF2α, and BK and with pain intensity assessed by VAS. BKB1R expression was also positively correlated with dysmenorrhea severity, supporting a link between BK/BKB1R and prostaglandin-mediated pain mechanisms, though the study is limited by its observational, cross-sectional design and reliance on correlations rather than direct mechanistic testing. This paper is centrally about endometriosis — specifically the involvement of bradykinin B1 receptor (BKB1R) and its association with prostaglandins in endometriosis-associated pain.

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Abstract

Endometriosis (EM), a benign aseptic inflammatory disease, is associated with the presence of endometrial foci. Pain, one of its typical symptoms, has been reported as a constant stressor, but the etiology and pathogenesis of EM‑associated pain are unclear. In the present study, eutopic and ectopic endometrium samples from women with EM (n=50) and normal endometrium samples from control subjects (n=20) were collected. Serum levels of prostaglandin E2 (PGE2), prostaglandin F2α (PGF2α) and bradykinin (BK) were measured using commercial ELISA kits. The expression of the BKB1 receptor (BKB1R) protein was evaluated by immunohistochemical staining and western blot assay. The mRNA expression of BKB1R was measured by reverse transcription‑quantitative PCR. The results revealed that there was a substantial increase in the protein and mRNA expression of BKB1R, as well as the release of PGE2, PGF2α and BK in the blood, in the EM group compared with that in the control group. Moreover, PGE2, PGF2α and BK levels were significantly correlated with each other, as well as with the pain intensity of EM. The increased expression levels of BKB1R protein and mRNA were positively correlated with the pain degree of EM. Thus, these data indicated that BK and BKB1R were involved in the pathological onset of EM‑associated pain and that they may play an important role in EM‑related pain by inducing PGE2 and PGF2α. The data indicate a potential new therapeutic target for EM‑related pain.

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endometriosis

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