Bromodomain-containing protein 4 contributes to chronic postsurgical pain via activating TLR4/NF-kappaB-dependent neuroinflammation

Abstract Background Chronic pain affects 1.5 billion individuals worldwide but remains woefully undertreated, particularly occurring in the populations undergoing surgical procedures. Increasing evidence indicates that epigenetic modifications are involved in the pathogenesis of chronic pain. This s...

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Main Authors: Ruichen Shu, Yuan Li, Zengli Zhang, Xuan Zhang, Shan Guan, Kaiyuan Wang, Yiqing Yin
Format: Article
Language:English
Published: BMC 2025-07-01
Series:BMC Anesthesiology
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Online Access:https://doi.org/10.1186/s12871-025-03216-6
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author Ruichen Shu
Yuan Li
Zengli Zhang
Xuan Zhang
Shan Guan
Kaiyuan Wang
Yiqing Yin
author_facet Ruichen Shu
Yuan Li
Zengli Zhang
Xuan Zhang
Shan Guan
Kaiyuan Wang
Yiqing Yin
author_sort Ruichen Shu
collection DOAJ
description Abstract Background Chronic pain affects 1.5 billion individuals worldwide but remains woefully undertreated, particularly occurring in the populations undergoing surgical procedures. Increasing evidence indicates that epigenetic modifications are involved in the pathogenesis of chronic pain. This study aimed to investigate the role of bromodomain-containing protein 4 (Brd4) in chronification of pain after surgery. Methods Male Sprague-Dawley rats were subjected to skin/muscle incision and retraction surgery to induce chronic postsurgical pain. Nociceptive thresholds and locomotor activity were assessed. The spinal cord was collected to detect the expressions of Brd4, toll-like receptor 4 (TLR4)/nuclear factor-kappaB (NF-κB) pathway, and proinflammatory cytokines and chemokines release. The BET inhibitor JQ1 was used to verify the contribution of Brd4 to chronic postsurgical pain. Results Significant upregulation of spinal Brd4 expression, accompanied by activation of the TLR4/NF-κB signaling cascade and increased release of proinflammatory mediators were presented in the rat model of chronic postsurgical pain. The BET inhibitor JQ1 prevented the development of chronic postsurgical pain in a dose-dependent manner. Moreover, JQ1 obviously suppressed the activation of TLR4 and the phosphorylation and translocation of NF-κB as well as subsequently cytokines and chemokines release, including IL-1β, IL-6, TNF-α, CXCL1, CXCL2 and CCL2. Conclusions The epigenetic regulator Brd4 initiates neuroinflammation in spinal cord through activating TLR4/NF-κB signaling pathway and enhancing cytokine and chemokines release, thereby contributing to the transition to chronic postsurgical pain. JQ1 halts chronic pain development, providing a novel therapy for patients at high risk of persistent pain.
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spelling doaj-art-0e14d6cdb6d546d2baee7b149b29c4102025-08-20T04:02:55ZengBMCBMC Anesthesiology1471-22532025-07-0125111010.1186/s12871-025-03216-6Bromodomain-containing protein 4 contributes to chronic postsurgical pain via activating TLR4/NF-kappaB-dependent neuroinflammationRuichen Shu0Yuan Li1Zengli Zhang2Xuan Zhang3Shan Guan4Kaiyuan Wang5Yiqing Yin6Department of Anesthesiology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin’s Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, State Key Laboratory of Druggability Evaluation and Systematic Translational MedicineDepartment of Anesthesiology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin’s Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, State Key Laboratory of Druggability Evaluation and Systematic Translational MedicineDepartment of Anesthesiology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin’s Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, State Key Laboratory of Druggability Evaluation and Systematic Translational MedicineDepartment of Anesthesiology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin’s Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, State Key Laboratory of Druggability Evaluation and Systematic Translational MedicineDepartment of Anesthesiology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin’s Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, State Key Laboratory of Druggability Evaluation and Systematic Translational MedicineDepartment of Anesthesiology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin’s Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, State Key Laboratory of Druggability Evaluation and Systematic Translational MedicineDepartment of Anesthesiology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin’s Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, State Key Laboratory of Druggability Evaluation and Systematic Translational MedicineAbstract Background Chronic pain affects 1.5 billion individuals worldwide but remains woefully undertreated, particularly occurring in the populations undergoing surgical procedures. Increasing evidence indicates that epigenetic modifications are involved in the pathogenesis of chronic pain. This study aimed to investigate the role of bromodomain-containing protein 4 (Brd4) in chronification of pain after surgery. Methods Male Sprague-Dawley rats were subjected to skin/muscle incision and retraction surgery to induce chronic postsurgical pain. Nociceptive thresholds and locomotor activity were assessed. The spinal cord was collected to detect the expressions of Brd4, toll-like receptor 4 (TLR4)/nuclear factor-kappaB (NF-κB) pathway, and proinflammatory cytokines and chemokines release. The BET inhibitor JQ1 was used to verify the contribution of Brd4 to chronic postsurgical pain. Results Significant upregulation of spinal Brd4 expression, accompanied by activation of the TLR4/NF-κB signaling cascade and increased release of proinflammatory mediators were presented in the rat model of chronic postsurgical pain. The BET inhibitor JQ1 prevented the development of chronic postsurgical pain in a dose-dependent manner. Moreover, JQ1 obviously suppressed the activation of TLR4 and the phosphorylation and translocation of NF-κB as well as subsequently cytokines and chemokines release, including IL-1β, IL-6, TNF-α, CXCL1, CXCL2 and CCL2. Conclusions The epigenetic regulator Brd4 initiates neuroinflammation in spinal cord through activating TLR4/NF-κB signaling pathway and enhancing cytokine and chemokines release, thereby contributing to the transition to chronic postsurgical pain. JQ1 halts chronic pain development, providing a novel therapy for patients at high risk of persistent pain.https://doi.org/10.1186/s12871-025-03216-6Chronic postsurgical painBrd4EpigeneticsNeuroinflammationNF-κB
spellingShingle Ruichen Shu
Yuan Li
Zengli Zhang
Xuan Zhang
Shan Guan
Kaiyuan Wang
Yiqing Yin
Bromodomain-containing protein 4 contributes to chronic postsurgical pain via activating TLR4/NF-kappaB-dependent neuroinflammation
BMC Anesthesiology
Chronic postsurgical pain
Brd4
Epigenetics
Neuroinflammation
NF-κB
title Bromodomain-containing protein 4 contributes to chronic postsurgical pain via activating TLR4/NF-kappaB-dependent neuroinflammation
title_full Bromodomain-containing protein 4 contributes to chronic postsurgical pain via activating TLR4/NF-kappaB-dependent neuroinflammation
title_fullStr Bromodomain-containing protein 4 contributes to chronic postsurgical pain via activating TLR4/NF-kappaB-dependent neuroinflammation
title_full_unstemmed Bromodomain-containing protein 4 contributes to chronic postsurgical pain via activating TLR4/NF-kappaB-dependent neuroinflammation
title_short Bromodomain-containing protein 4 contributes to chronic postsurgical pain via activating TLR4/NF-kappaB-dependent neuroinflammation
title_sort bromodomain containing protein 4 contributes to chronic postsurgical pain via activating tlr4 nf kappab dependent neuroinflammation
topic Chronic postsurgical pain
Brd4
Epigenetics
Neuroinflammation
NF-κB
url https://doi.org/10.1186/s12871-025-03216-6
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