scholarly journals Dietary polyphenols as a safe and novel intervention for modulating pain associated with intervertebral disc degeneration in an in-vivo rat model

PLoS ONE ◽  
2019 ◽  
Vol 14 (10) ◽  
pp. e0223435 ◽  
Author(s):  
Alon Lai ◽  
Lap Ho ◽  
Thomas W. Evashwick-Rogler ◽  
Hironobu Watanabe ◽  
Jonathan Salandra ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Rat Model ◽  
Intervertebral Disc Degeneration ◽  
Dietary Polyphenols

scholarly journals Correction: Dietary polyphenols as a safe and novel intervention for modulating pain associated with intervertebral disc degeneration in an in-vivo rat model

PLoS ONE ◽  
2019 ◽  
Vol 14 (11) ◽  
pp. e0225674
Author(s):  
Alon Lai ◽  
Lap Ho ◽  
Thomas W. Evashwick-Rogler ◽  
Hironobu Watanabe ◽  
Jonathan Salandra ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Rat Model ◽  
Intervertebral Disc Degeneration ◽  
Dietary Polyphenols

Cervical Intervertebral Disc Degeneration Induced by Unbalanced Dynamic and Static Forces: A Novel In Vivo Rat Model

Spine ◽  
2006 ◽  
Vol 31 (14) ◽  
pp. 1532-1538 ◽  
Author(s):  
Yong-Jun Wang ◽  
Qi Shi ◽  
W W. Lu ◽  
K C. M. Cheung ◽  
Michael Darowish ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Rat Model ◽  
Intervertebral Disc Degeneration

scholarly journals CircERCC2 ameliorated intervertebral disc degeneration by regulating mitophagy and apoptosis through miR-182-5p/SIRT1 axis

2019 ◽  
Vol 10 (10) ◽  
Author(s):  
Lin Xie ◽  
Weibo Huang ◽  
Zhenhua Fang ◽  
Fan Ding ◽  
Fei Zou ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Rat Model ◽  
Intervertebral Disc Degeneration ◽  
Circular Rnas ◽  
Tert Butyl Hydroperoxide ◽  
In Vitro Treatment

Abstract The molecular mechanism of intervertebral disc degeneration (IVDD) remains unclear. This study aimed to investigate the role of circular RNAs (circRNAs) in the pathogenesis of IVDD. We sued nucleus pulposus (NP) tissues of patients, tert-butyl hydroperoxide (TBHP) stimulated NP cells (NPCs), and IVDD rat model to explore the interaction between circERCC2 and miR-182-5p/SIRT1 axis. The results showed that downregulation of circERCC2 increased the level of miR-182-5p and decreased the level of SIRT1 in degenerative NP tissues in vivo as well as in TBHP-stimulated NPCs in vitro. Treatment of SIRT1-si activated apoptosis and inhibited mitophagy. Moreover, miR-182-5p-si could regulate the mitophagy and the apoptosis of NPCs by targeting SIRT1. The effects of circERCC2 on NPCs and IVDD rat model were mediated by miR-182-5p/SIRT1 axis. In conclusion, this study provides the first evidence that circERCC2 could ameliorate IVDD through miR-182-5p/SIRT1 axis by activating mitophagy and inhibiting apoptosis, and suggests that circERCC2 is a potentially effective therapeutic target for IVDD.

scholarly journals An in vivo study of the effect of c-Jun on intervertebral disc degeneration in rats

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 4320-4330
Author(s):  
Ming Lei ◽  
Kangcheng Zhao ◽  
Wenbin Hua ◽  
Kun Wang ◽  
Shuai Li ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
In Vivo Study

scholarly journals Expression of miR-195 and its target gene Bcl-2 in human intervertebral disc degeneration and their effects on nucleus pulposus cell apoptosis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Xue-Lin Lin ◽  
Zhao-Yun Zheng ◽  
Qing-Shan Zhang ◽  
Zhen Zhang ◽  
You-Zhi An
Keyword(s):  
Cell Proliferation ◽  
Intervertebral Disc ◽  
Nucleus Pulposus ◽  
Disc Degeneration ◽  
Rat Model ◽  
Cell Apoptosis ◽  
Intervertebral Disc Degeneration ◽  
Target Gene ◽  
Blank Group ◽  
Tnf Α

Abstract Objective To investigate the expression of miR-195 and its target gene Bcl-2 in intervertebral disc degeneration (IVDD) and its effect on nucleus pulposus (NP) cell apoptosis. Methods The expressions of miR-195 and Bcl-2 in NP tissues of IVDD patients were quantified by qRT-PCR and western blotting, respectively. NP cells were divided into blank group, TNF-α group, TNF-α + miR-NC group, TNF-α + siBcl-2 group, and TNF-α + miR-195 inhibitors + siBcl-2 group. Cell proliferation was detected by MTT assay, cell apoptosis evaluated by flow cytometry, and mitochondrial membrane potential (MMP) tested by JC-1 staining. Moreover, the function of miR-195 on IVDD in vivo was investigated using a puncture-induced IVDD rat model. Results IVDD patients had significantly increased miR-195 expression and decreased Bcl-2 protein expression in NP tissues. The expression of miR-195 was negatively correlated with the expression of Bcl-2 in IVDD patients. Dual-luciferase reporter gene assay indicated that Bcl-2 was a target gene of miR-195. In comparison with blank group, TNF-α group showed decreased cell proliferation and MMP, increased cell apoptosis, upregulated expression of miR-195, Bax, and cleaved caspase 3, and downregulated Bcl-2 protein, while these changes were attenuated by miR-195 inhibitors. Additionally, siBcl-2 can reverse the protective effect of miR-195 inhibitors on TNF-α-induced NP cells. Besides, inhibition of miR-195 alleviated IVDD degeneration and NP cell apoptosis in the rat model. Conclusion MiR-195 was significantly upregulated in NP tissues of IVDD patients, and inhibition of miR-195 could protect human NP cells from TNF-α-induced apoptosis via upregulation of Bcl-2.

Recovery of Intervertebral Disc Degeneration Post Enzymatic Treatment is Mediated by Matrix Metalloproteinases

2011 ◽  
Author(s):  
Nadeen Chahine ◽  
Nate Stetson ◽  
Neena Rajan ◽  
Daniel Grande ◽  
Mitchell Levine
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Enzymatic Degradation ◽  
Intervertebral Disc Degeneration ◽  
Biomechanical Properties ◽  
Enzymatic Treatment ◽  
Disc Injury ◽  
Herniated Discs ◽  
Dose Dependent

Enzymatic degradation of the intervertebral disc (IVD) with chondroitinase ABC (ChABC) reduces proteoglycan content of the IVD, thus simulating the GAG loss seen clinically in patients suffering from disc degeneration. This approach has been employed in models of disc injury in rats, rabbits and goats when administered over a large range of dosages [1–3]. Moreover, ChABC has also been used to induce repair of herniated discs in rabbits via chemonucleolysis [4, 5]. Despite the effectiveness of ChABC treatment to reduce the GAG content of the IVD, several recent studies including our own, have shown that this GAG loss is reversible at extended time points post enzymatic treatment [2,6,7]. The goal of the current study is to examine the dose dependent response of IVDs to degradation by ChABC in vivo. We hypothesize that administration of ChABC will result in dose dependent GAG loss and reduced mechanical properties. We administered ChABC at 0.1 U/ml, 1.0 U/ml and 10 U/ml and examined the changes in biomechanical properties, biochemical content, and gene expression in order to examine the biophysical and molecular mechanism by which GAG loss occurs in this model.

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