Restoration of Autophagic Flux Rescues Oxidative Damage and Mitochondrial Dysfunction to Protect against Intervertebral Disc Degeneration
Identifieur interne : 000E65 ( Ncbi/Curation ); précédent : 000E64; suivant : 000E66Restoration of Autophagic Flux Rescues Oxidative Damage and Mitochondrial Dysfunction to Protect against Intervertebral Disc Degeneration
Auteurs : Liang Kang [République populaire de Chine] ; Qian Xiang [République populaire de Chine] ; Shengfeng Zhan [République populaire de Chine] ; Yu Song [République populaire de Chine] ; Kun Wang [République populaire de Chine] ; Kangcheng Zhao [République populaire de Chine] ; Shuai Li [République populaire de Chine] ; Zengwu Shao [République populaire de Chine] ; Cao Yang [République populaire de Chine] ; Yukun Zhang [République populaire de Chine]Source :
- Oxidative Medicine and Cellular Longevity [ 1942-0900 ] ; 2019.
Abstract
Oxidative stress-induced mitochondrial dysfunction and nucleus pulposus (NP) cell apoptosis play crucial roles in the development of intervertebral disc degeneration (IDD). Increasing studies have shown that interventions targeting impaired autophagic flux can maintain cellular homeostasis by relieving oxidative damage. Here, we investigated the effect of curcumin (CUR), a known autophagy activator, on IDD
Url:
DOI: 10.1155/2019/7810320
PubMed: 31976028
PubMed Central: 6954474
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PMC:6954474Le document en format XML
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<author><name sortKey="Zhang, Yukun" sort="Zhang, Yukun" uniqKey="Zhang Y" first="Yukun" last="Zhang">Yukun Zhang</name>
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<front><div type="abstract" xml:lang="en"><p>Oxidative stress-induced mitochondrial dysfunction and nucleus pulposus (NP) cell apoptosis play crucial roles in the development of intervertebral disc degeneration (IDD). Increasing studies have shown that interventions targeting impaired autophagic flux can maintain cellular homeostasis by relieving oxidative damage. Here, we investigated the effect of curcumin (CUR), a known autophagy activator, on IDD <italic>in vitro</italic>
and <italic>in vivo</italic>
. CUR suppressed <italic>tert</italic>
-butyl hydroperoxide- (TBHP-) induced oxidative stress and mitochondrial dysfunction and thereby inhibited human NP cell apoptosis, senescence, and ECM degradation. CUR treatment induced autophagy and enhanced autophagic flux in an AMPK/mTOR/ULK1-dependent manner. Notably, CUR alleviated TBHP-induced interruption of autophagosome-lysosome fusion and impairment of lysosomal function and thus contributed to the restoration of blocked autophagic clearance. These protective effects of CUR in TBHP-stimulated human NP cells resembled the effects produced by the autophagy inducer rapamycin, but the effects were partially eliminated by 3-methyladenine- and compound C-mediated inhibition of autophagy initiation or chloroquine-mediated obstruction of autophagic flux. Lastly, CUR also exerted a protective effect against puncture-induced IDD progression <italic>in vivo</italic>
. Our results showed that suppression of excessive ROS production and mitochondrial dysfunction through enhancement of autophagy coupled with restoration of autophagic flux ameliorated TBHP-induced human NP cell apoptosis, senescence, and ECM degradation. Thus, maintenance of the proper functioning of autophagy represents a promising therapeutic strategy for IDD, and CUR might serve as an effective therapeutic agent for IDD.</p>
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