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This study evaluates Friedelin (FD) and its anti-inflammatory action on IVDD by examining the NF-κB signalling pathway. In vivo cervical disc tissue from mice with cervical spine instability and in vitro assays with nucleus pulposus cells show that FD reduces NP degeneration and inflammatory cytokine production by promoting autophagic clearance of p65 and inhibiting NF-κB activation, involving p65 phosphorylation control and RNF182-mediated 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Ameliorates Nucleus Pulposus Inflammation by Increasing p65 Autophagic Degradation to Inhibit NF-κB Signalling Pathway  \nKewu Tu1 | Dongteng Liao2 | Zhaomou Chen2 | Zhenyu Wang3 | Kun Zhao2 | Hongyu Zhong4 | Shimin Wu5 | Huiyin Zhu5 | Jinming Xu6 | Beidi Zhou7 | Xiangheng Dai1 | Qiang Wu1   \n1Department of Spinal Surgery, Shaoguan First People's Hospital, Guangdong Medical University, Shaoguan, China | 2The First School of Clinical Medicine, Guangdong Medical University, Zhanjiang, China | 3Department of Orthopaedics, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, China | 4Second Clinical School, Guangzhou Medical University, Guangzhou, China | 5Medical School of Shaoguan University, Shaoguan, China | 6Department of Joint, Sports Medicine & Pediatric Orthopedics, Shaoguan First People's Hospital, Guangdong Medical University, Shaoguan,  \nChina | 7Department of Prevention and Health Care, Shaoguan First People's Hospital, Guangdong Medical University, Shaoguan, China Correspondence: Xiangheng Dai ([daixiangheng@sgu.edu.cn](daixiangheng@sgu.edu.cn)) | Qiang Wu ([sgwuqiang@sgu.edu.cn](sgwuqiang@sgu.edu.cn))  \nReceived: 19 October 2025 | Revised: 23 November 2025 | Accepted: 9 December 2025  \nKeywords: Friedelin | inflammation | intervertebral disc degeneration | NF-κB signalling | RNF182  \nABSTRACT  \nIntervertebral disc degeneration (IVDD) is a prevalent disorder associated with chronic inflammation, significantly affecting spinal health and general quality of life. This study examines the anti-inflammatory properties of Friedelin (FD) and its impact on the NF-κB signalling pathway in relation to IVDD. In vivo experiments utilising cervical intervertebral disc tissue from mice exhibiting cervical spine instability and in vitro assays with nucleus pulposus (NP) cells revealed that FD treatment significantly diminished NP degeneration and inflammatory cytokine production, concurrently inhibiting NF-κB activation. FD triggered autophagic clearance of p65, reducing inflammatory cytokine output. This effect was mediated by selective inhibition of p65 phosphorylation, independent of IKK activity, highlighting its targeted action on NF-κB signalling. Moreover, FD enhanced the association between p65 and the E3 ubiquitin ligase RNF182, facilitating p65 degradation via autophagy. The findings indicate that FD mitigates IVDD by diminishing NP degradation and inflammation while also presenting a potential therapeutic strategy that targets the NF-κB signalling pathway through autophagic processes.  \n1 | Introduction  \nIntervertebral disc degeneration (IVDD) is a common ailment that considerably affects spinal health and overall quality of life [1] . This condition entails the degeneration of intervertebral discs, potentially leading to persistent pain, incapacity and reduced mobility [2] . Recent studies underscore that chronic NP inflammation drives IVDD progression [3–5] . Despite this understanding, the specific molecular mechanisms underlying the inflammatory response in IVDD remain poorly defined and  \neffective therapeutic options are limited [6, 7] . This highlightsa significant gap in current knowledge and underscores the urgent need for further research to develop better treatments.  \nRecent investigations indicate that intervertebral discs undergo several biochemical alterations during degeneration, including changes in the extracellular matrix and heightened production of inflammatory cytokines [8, 9] . The nuclear factor kappa B (NF-κB) signalling pathway is a vital component in this process, recognised as a fundamental regulator of inflammation in IVDD  \n\n| Kewu Tu, Dongteng Liao, Zhaomou Chen and Zhenyu Wang contributed equally to this work. |\n| --- |\n| This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the origin","cbCaiiVN510cmHxn","https://ap.wps.com/l/cbCaiiVN510cmHxn","pdf",6675060,12,"English","# Introduction\n## Intervertebral disc degeneration and inflammation\n## NF-κB signalling in IVDD\n## Rationale for Friedelin and study aims","[{\"question\":\"What condition does this research target?\",\"answer\":\"The study targets intervertebral disc degeneration (IVDD), a disorder driven in part by chronic inflammation affecting spinal health.\"},{\"question\":\"How does Friedelin (FD) influence the NF-κB pathway?\",\"answer\":\"FD inhibits NF-κB activation by triggering autophagic clearance of p65, including selective suppression of p65 phosphorylation.\"},{\"question\":\"What mechanism links p65 degradation to FD treatment?\",\"answer\":\"FD increases the association between p65 and the E3 ubiquitin ligase RNF182, facilitating p65 degradation via autophagy independent of IKK activity.\"}]","Friedelin Ameliorates Nucleus Pulposus Inflammation by Increasing p65 Autophagic Degradation to Inhibit NF-κB Signalling Pathway | PDF",1790752870]