scholarly journals Time-Course Investigation of Intervertebral Disc Degeneration Induced by Different Sizes of Needle Punctures in Rat Tail Disc

2018 ◽  
Vol 24 ◽  
pp. 6456-6465 ◽  
Author(s):  
Tao Chen ◽  
Xiaofei Cheng ◽  
Jingcheng Wang ◽  
Xinmin Feng ◽  
Liang Zhang
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Time Course ◽  
Rat Tail

Time course investigation of intervertebral disc degeneration in a rat-tail puncture model

Life Sciences ◽  
2016 ◽  
Vol 156 ◽  
pp. 15-20 ◽  
Author(s):  
Chia-Hsian Chen ◽  
Chang-Jung Chiang ◽  
Lien-Chen Wu ◽  
Chih-Hong Yang ◽  
Yi-Jie Kuo ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Time Course ◽  
Puncture Model ◽  
Rat Tail

scholarly journals Involvement of Autophagy in Rat Tail Static Compression-Induced Intervertebral Disc Degeneration and Notochordal Cell Disappearance

2021 ◽  
Vol 22 (11) ◽  
pp. 5648
Author(s):  
Takashi Yurube ◽  
Hiroaki Hirata ◽  
Masaaki Ito ◽  
Yoshiki Terashima ◽  
Yuji Kakiuchi ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Time Course ◽  
The Body ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Autophagic Flux ◽  
Static Compression ◽  
Notochordal Cell ◽  
Notochordal Cells ◽  
Rat Tail

The intervertebral disc is the largest avascular low-nutrient organ in the body. Thus, resident cells may utilize autophagy, a stress-response survival mechanism, by self-digesting and recycling damaged components. Our objective was to elucidate the involvement of autophagy in rat experimental disc degeneration. In vitro, the comparison between human and rat disc nucleus pulposus (NP) and annulus fibrosus (AF) cells found increased autophagic flux under serum deprivation rather in humans than in rats and in NP cells than in AF cells of rats (n = 6). In vivo, time-course Western blotting showed more distinct basal autophagy in rat tail disc NP tissues than in AF tissues; however, both decreased under sustained static compression (n = 24). Then, immunohistochemistry displayed abundant autophagy-related protein expression in large vacuolated disc NP notochordal cells of sham rats. Under temporary static compression (n = 18), multi-color immunofluorescence further identified rapidly decreased brachyury-positive notochordal cells with robust expression of autophagic microtubule-associated protein 1 light chain 3 (LC3) and transiently increased brachyury-negative non-notochordal cells with weaker LC3 expression. Notably, terminal deoxynucleotidyl transferase dUTP nick end labeling-positive apoptotic death was predominant in brachyury-negative non-notochordal cells. Based on the observed notochordal cell autophagy impairment and non-notochordal cell apoptosis induction under unphysiological mechanical loading, further investigation is warranted to clarify possible autophagy-induced protection against notochordal cell disappearance, the earliest sign of disc degeneration, through limiting apoptosis.

Establishment of intervertebral disc degeneration model induced by ischemic sub-endplate in rat tail

2015 ◽  
Vol 15 (5) ◽  
pp. 1050-1059 ◽  
Author(s):  
Wei Yuan ◽  
Wu Che ◽  
Yun-Qi Jiang ◽  
Feng-Lai Yuan ◽  
Hui-Ren Wang ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Rat Tail

Static Compression Induces ECM Remodeling and Integrin α2β1 Expression and Signaling in a Rat Tail Caudal Intervertebral Disc Degeneration Model

Spine ◽  
2017 ◽  
Vol 42 (8) ◽  
pp. E448-E458 ◽  
Author(s):  
ZhanJun Yan ◽  
YouDong Pan ◽  
ShiHui Wang ◽  
MaoHua Cheng ◽  
HongMei Kong ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Static Compression ◽  
Ecm Remodeling ◽  
Rat Tail

scholarly journals Effect of sIL-13Rα2-Fc on the progression of rat tail intervertebral disc degeneration

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Xin Wang ◽  
Junhao Sun ◽  
Jianshi Tan ◽  
Pengzhong Fang ◽  
Jinlei Chen ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Rat Tail

The Effect of Timing of rhBMP-2 Injection on Intervertebral Disc Degeneration in a Rat Tail Model

2012 ◽  
Vol 12 (9) ◽  
pp. S74
Author(s):  
Scott R. Montgomery ◽  
Hirokazu Inoue ◽  
Tuncay Kaner ◽  
Bayan G. Aghdasi ◽  
Yanlin Tan ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Rat Tail Model ◽  
Rat Tail

scholarly journals Quercetin Alleviates Intervertebral Disc Degeneration by Modulating p38 MAPK-Mediated Autophagy

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Shuwen Zhang ◽  
Weidong Liang ◽  
Yakefu Abulizi ◽  
Tao Xu ◽  
Rui Cao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intervertebral Disc ◽  
Protective Effect ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Mapk Signaling ◽  
Therapeutic Effects ◽  
Rat Tail

Intervertebral disc degeneration (IVDD) is a degenerative and chronic spinal disorder often associated with the older population. Oxidative stress is a major pathogenic factor of aging that results in the apoptosis of nucleus pulposus cells (NPCs) and extracellular matrix (ECM) degradation. Quercetin (QUE), a naturally occurring flavonoid with antioxidant and anti-inflammatory properties, has been studied in research on degenerative diseases. However, the potential effects and mechanisms of action of QUE on IVDD remain unclear. In this study, the effects of QUE on antiapoptosis and ECM metabolism were firstly investigated in TBHP-treated NPCs. Meanwhile, the autophagy inhibitor, 3-MA, and p38 MAPK inhibitor, SB203580, were used in subsequent TBHP-induced NPC experiments to determine whether QUE exerted its protective effects through autophagy and the p38 MAPK/mTOR signaling pathway. Finally, the therapeutic effects of QUE were confirmed in vivo using a rat tail needle puncture-induced model of IVDD. We found that QUE treatment significantly alleviated oxidative stress-decreased cell viability and intracellular ROS levels in NPCs treated with TBHP. Furthermore, treatment with QUE led to a decrease in apoptosis as measured by decreased Bax and increased Bcl-2 expression and PE/7-AAD flow cytometry analysis. QUE also promoted ECM stability as measured by increased collagen II and aggrecan and decreased MMP13 levels. Our results also showed that QUE promoted the expression of autophagy markers beclin-1, LC3-II/I, and decreased p62. Inhibition of autophagy by inhibitor 3-MA may partially reverse the protective effect of QUE on apoptosis and ECM degeneration, indicating that autophagy was involved in the protective effect of QUE in NPCs. Further study confirmed that QUE partially inhibited the p38 MAPK signaling pathway and inhibition of p38 MAPK by SB203580 activated autophagy, indicating that QUE protected NPCs against apoptosis and prevented ECM degeneration via the p38 MAPK-autophagy pathway. Finally, using a rat tail puncture-induced model of IVDD, we confirmed that QUE had a protective effect against IVDD. Our results suggest that QUE could prevent IVDD by modulating p38 MAPK-mediated autophagy and, therefore, is a potential therapeutic strategy in the treatment of IVDD.

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