Frontiers in Cell and Developmental Biology (Jan 2022)
Apigenin Alleviates Intervertebral Disc Degeneration via Restoring Autophagy Flux in Nucleus Pulposus Cells
- Chenglong Xie,
- Chenglong Xie,
- Chenglong Xie,
- Yifeng Shi,
- Yifeng Shi,
- Yifeng Shi,
- Zuoxi Chen,
- Xin Zhou,
- Xin Zhou,
- Peng Luo,
- Peng Luo,
- Peng Luo,
- Chenxuan Hong,
- Chenxuan Hong,
- Chenxuan Hong,
- Naifeng Tian,
- Naifeng Tian,
- Naifeng Tian,
- Yaosen Wu,
- Yaosen Wu,
- Yaosen Wu,
- Yifei Zhou,
- Yifei Zhou,
- Yifei Zhou,
- Yan Lin,
- Yan Lin,
- Yan Lin,
- Haicheng Dou,
- Haicheng Dou,
- Haicheng Dou,
- Aimin Wu,
- Aimin Wu,
- Aimin Wu,
- Qishan Huang,
- Qishan Huang,
- Qishan Huang,
- Xiaolei Zhang,
- Xiaolei Zhang,
- Xiaolei Zhang,
- Xiaolei Zhang,
- Xiangyang Wang,
- Xiangyang Wang,
- Xiangyang Wang
Affiliations
- Chenglong Xie
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Chenglong Xie
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Chenglong Xie
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Yifeng Shi
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Yifeng Shi
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Yifeng Shi
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Zuoxi Chen
- Department of Orthopaedics, Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine, Wenzhou, China
- Xin Zhou
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Xin Zhou
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Peng Luo
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Peng Luo
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Peng Luo
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Chenxuan Hong
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Chenxuan Hong
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Chenxuan Hong
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Naifeng Tian
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Naifeng Tian
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Naifeng Tian
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Yaosen Wu
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Yaosen Wu
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Yaosen Wu
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Yifei Zhou
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Yifei Zhou
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Yifei Zhou
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Yan Lin
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Yan Lin
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Yan Lin
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Haicheng Dou
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Haicheng Dou
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Haicheng Dou
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Aimin Wu
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Aimin Wu
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Aimin Wu
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Qishan Huang
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Qishan Huang
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Qishan Huang
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Xiaolei Zhang
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Xiaolei Zhang
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Xiaolei Zhang
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- Xiaolei Zhang
- Chinese Orthopaedic Regenerative Medicine Society, Hangzhou, China
- Xiangyang Wang
- Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, China
- Xiangyang Wang
- Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou, China
- Xiangyang Wang
- The Second School of Medicine, Wenzhou Medical University, Wenzhou, China
- DOI
- https://doi.org/10.3389/fcell.2021.787278
- Journal volume & issue
-
Vol. 9
Abstract
Oxidative stress–induced apoptosis and senescence of nucleus pulposus (NP) cells play a crucial role in the progression of intervertebral disc degeneration (IVDD). Accumulation of studies has shown that activated autophagy and enhanced autophagic flux can alleviate IVDD. In this study, we explored the effects of apigenin on IVDD in vitro and in vivo. Apigenin was found to inhibit tert-butyl hydroperoxide (TBHP)–induced apoptosis, senescence, and ECM degradation in NP cells. In addition, apigenin treatment can restore the autophagic flux blockage caused by TBHP. Mechanistically, we found that TBHP may induce autophagosome and lysosome fusion interruption and lysosomal dysfunction, while apigenin alleviates these phenomena by promoting the nuclear translocation of TFEB via the AMPK/mTOR signaling pathway. Furthermore, apigenin also exerts a protective effect against the progression of IVDD in the puncture-induced rat model. Taken together, these findings indicate that apigenin protects NP cells against TBHP-induced apoptosis, senescence, and ECM degradation via restoration of autophagic flux in vitro, and it also ameliorates IVDD progression in rats in vivo, demonstrating its potential for serving as an effective therapeutic agent for IVDD.
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