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Abstract Title:

Urolithin A-induced mitophagy suppresses apoptosis and attenuates intervertebral disc degeneration via the AMPK signaling pathway.

Abstract Source:

Free Radic Biol Med. 2020 Feb 24 ;150:109-119. Epub 2020 Feb 24. PMID: 32105828

Abstract Author(s):

Jialiang Lin, Jinru Zhuge, Xuanqi Zheng, Yuhao Wu, Zengjie Zhang, Tianzhen Xu, Zaher Meftah, Hongming Xu, Yaosen Wu, Naifeng Tian, Weiyang Gao, Yifei Zhou, Xiaolei Zhang, Xiangyang Wang

Article Affiliation:

Jialiang Lin

Abstract:

Intervertebral disc degeneration (IDD) is a major cause of low back pain (LBP), and effective therapies are still lacking. Previous studies reported that mitochondrial dysfunction contributes to apoptosis, and urolithin A (UA) specifically induces mitophagy. Herein, we aimed to investigate the protective effect of UA-induced mitophagy on tert-butyl hydroperoxide (TBHP)-induced apoptosis in nucleus pulposus (NP) cells in vitro and a rat model of IDD in vivo. Mitochondrial function, apoptosis, and mitophagy were measured in UA-treated NP cells by western blotting and immunofluorescence; the therapeutic effects of UA on IDD were assessed in rats with puncture-induced IDD. The results showed that UA could activate mitophagy in primary NP cells, and UA treatment inhibited TBHP-induced mitochondrial dysfunction and the intrinsic apoptosis pathway. Mechanistically, we revealed that UA promoted mitophagy by activating AMPK signaling in TBHP-induced NP cells. In vivo, UA was shown to effectively alleviate the progression of puncture-induced IDD in rats. Taken together, our results suggest that UA could be a novel and effective therapeutic strategy for IDD.

Study Type : Animal Study

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