TXNIP公司
维拉帕米
体内
上睑下垂
药理学
活性氧
炎症体
医学
细胞生物学
生物
氧化应激
免疫学
炎症
内科学
硫氧还蛋白
生物技术
钙
作者
Yan Chen,Xiankun Cao,Bin Pan,Han Du,Baixing Li,Xiaobin Yang,Xuzhuo Chen,Xin Wang,Ting Zhou,An Qin,Changqing Zhao,Jie Zhao
标识
DOI:10.1016/j.intimp.2023.110789
摘要
Low back pain is usually caused by intervertebral disc degeneration (IVDD), during which the involvement of oxidation system imbalance and inflammasome activation cannot be neglected. In this study, we aimed to validate the expression level of TXNIP in IVDD and investigate the function and potential mechanism of action of verapamil. TXNIP is upregulated in the degenerate nucleus pulposus in both humans and rats, as well as in tert-butyl hydroperoxide (TBHP)-stimulated nucleus pulposus cells. Administration of verapamil, a classic clinical drug, mitigated the TBHP-induced overproduction of reactive oxygen species and activation of the NLRP3 inflammasome, thus protecting cells from pyroptosis, apoptosis, and extracellular matrix degradation. The Nrf2/TXNIP/NLRP3 axis plays a major role in verapamail-mediated protection. In vivo, a puncture-induced IVDD rat model was constructed, and we found that verapamil delayed the development of IVDD at both the imaging and histological levels. In summary, our results indicate the potential therapeutic effects and mechanisms of action of verapamil in the treatment of IVDD.
科研通智能强力驱动
Strongly Powered by AbleSci AI