椎间盘
变性(医学)
核心
缓激肽
化学
细胞生物学
医学
解剖
病理
生物
生物化学
受体
作者
Xiaoming Qiu,Chaoran Ma,Zhangbin Luo,Yibao Zhang,Jihe Kang,Daxue Zhu,Zhaoheng Wang,Lei Li,Ziyan Wei,Zhuanping Wang,Xuewen. Kang
标识
DOI:10.1016/j.intimp.2024.112161
摘要
Intervertebral disc degeneration (IVDD) is a leading cause of degenerative spinal disorders, involving complex biological processes. This study investigates the role of the kallikrein-kinin system (KKS) in IVDD, focusing on the protective effects of bradykinin (BK) on nucleus pulposus cells (NPCs) under oxidative stress. Clinical specimens were collected, and experiments were conducted using human and rat primary NPCs to elucidate BK's impact on tert-butyl hydroperoxide (TBHP)-induced oxidative stress and damage. The results demonstrate that BK significantly inhibits TBHP-induced NPC apoptosis and restores mitochondrial function. Further analysis reveals that this protective effect is mediated through the BK receptor 2 (B2R) and its downstream PI3K/AKT pathway. Additionally, BK/PLGA sustained-release microspheres were developed and validated in a rat model, highlighting their potential therapeutic efficacy for IVDD. Overall, this study sheds light on the crucial role of the KKS in IVDD pathogenesis and suggests targeting the B2R as a promising therapeutic strategy to delay IVDD progression and promote disc regeneration.
科研通智能强力驱动
Strongly Powered by AbleSci AI