Restoration of Autophagic Flux Rescues Oxidative Damage and Mitochondrial Dysfunction to Protect against Intervertebral Disc Degeneration

المؤلفون المشاركون

Kang, Liang
Xiang, Qian
Zhan, Shengfeng
Song, Yu
Wang, Kun
Zhao, Kangcheng
Li, Shuai
Shao, Zengwu
Yang, Cao
Zhang, Yukun

المصدر

Oxidative Medicine and Cellular Longevity

العدد

المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-27، 27ص.

الناشر

Hindawi Publishing Corporation

تاريخ النشر

2019-12-30

دولة النشر

مصر

عدد الصفحات

27

التخصصات الرئيسية

الأحياء

الملخص EN

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 in vitro and in vivo.

CUR suppressed tert-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 in vivo.

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.

نمط استشهاد جمعية علماء النفس الأمريكية (APA)

Kang, Liang& Xiang, Qian& Zhan, Shengfeng& Song, Yu& Wang, Kun& Zhao, Kangcheng…[et al.]. 2019. Restoration of Autophagic Flux Rescues Oxidative Damage and Mitochondrial Dysfunction to Protect against Intervertebral Disc Degeneration. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-27.
https://search.emarefa.net/detail/BIM-1205255

نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)

Kang, Liang…[et al.]. Restoration of Autophagic Flux Rescues Oxidative Damage and Mitochondrial Dysfunction to Protect against Intervertebral Disc Degeneration. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-27.
https://search.emarefa.net/detail/BIM-1205255

نمط استشهاد الجمعية الطبية الأمريكية (AMA)

Kang, Liang& Xiang, Qian& Zhan, Shengfeng& Song, Yu& Wang, Kun& Zhao, Kangcheng…[et al.]. Restoration of Autophagic Flux Rescues Oxidative Damage and Mitochondrial Dysfunction to Protect against Intervertebral Disc Degeneration. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-27.
https://search.emarefa.net/detail/BIM-1205255

نوع البيانات

مقالات

لغة النص

الإنجليزية

الملاحظات

Includes bibliographical references

رقم السجل

BIM-1205255