The effects of ferulic acid on nucleus pulposus cells under hydrogen peroxide-induced oxidative stress

2011 ◽  
Vol 46 (8) ◽  
pp. 1670-1677 ◽  
Author(s):  
Yung-Hsin Cheng ◽  
Shu-Hua Yang ◽  
Kai-Chiang Yang ◽  
Moon-Pei Chen ◽  
Feng-Huei Lin
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Ferulic Acid ◽  
Nucleus Pulposus ◽  
Nucleus Pulposus Cells

Melatonin resists oxidative stress-induced apoptosis in nucleus pulposus cells

Life Sciences ◽  
2018 ◽  
Vol 199 ◽  
pp. 122-130 ◽  
Author(s):  
Ruijun He ◽  
Min Cui ◽  
Hui Lin ◽  
Lei Zhao ◽  
Jiayu Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nucleus Pulposus ◽  
Nucleus Pulposus Cells ◽  
Induced Apoptosis

scholarly journals Caveolin-1 regulates oxidative stress-induced senescence in nucleus pulposus cells primarily via the p53/p21 signaling pathway in vitro

2017 ◽  
Vol 16 (6) ◽  
pp. 9521-9527 ◽  
Author(s):  
Lei Ding ◽  
Qingmin Zeng ◽  
Jingping Wu ◽  
Defang Li ◽  
Houlei Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Nucleus Pulposus ◽  
Nucleus Pulposus Cells ◽  
Caveolin 1

Sodium butyrate protects against oxidative stress in human nucleus pulposus cells via elevating PPARγ-regulated Klotho expression

2020 ◽  
Vol 85 ◽  
pp. 106657 ◽  
Author(s):  
Xinxin Liu ◽  
Chang Jiang ◽  
Guanghua Liu ◽  
Ping Wang ◽  
Mingfang Shi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nucleus Pulposus ◽  
Sodium Butyrate ◽  
Nucleus Pulposus Cells

Attenuating Oxidative Stress Via Oxalate Ester-Containing Ferulic Acid-Based Poly(anhydride-esters) that Scavenge Hydrogen Peroxide

2015 ◽  
Vol 217 (1) ◽  
pp. 108-114 ◽  
Author(s):  
Jonathan J. Faig ◽  
Sarah Klein ◽  
Michelle A. Ouimet ◽  
Weiling Yu ◽  
Kathryn E. Uhrich
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Ferulic Acid

scholarly journals CRISPR/dCas9-Mediated Parkin Inhibition Impairs Mitophagy and Aggravates Apoptosis of Rat Nucleus Pulposus Cells Under Oxidative Stress

2021 ◽  
Vol 8 ◽  
Author(s):  
Tao Lan ◽  
Yu-chen Zheng ◽  
Ning-dao Li ◽  
Xiao-sheng Chen ◽  
Zhe Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nucleus Pulposus ◽  
Pathological Condition ◽  
Protective Role ◽  
Intervertebral Disk ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Regulation Mechanism ◽  
Nucleus Pulposus Cells ◽  
Induced Apoptosis ◽  
Design And Methods

ObjectiveThe aim of this study is to explore the role of Parkin in intervertebral disk degeneration (IDD) and its mitophagy regulation mechanism.Study design and methodsRat nucleus pulposus (NP) cells were stimulated with hydrogen peroxide (H2O2) to a mimic pathological condition. Apoptosis and mitophagy were assessed by Western blot, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and immunofluorescence staining. The CRISPR–dCas9–KRAB system was used to silence the expression of Parkin.ResultIn this study, we found that Parkin was downregulated in rat NP cells under oxidative stress. In addition, treatment with H2O2 resulted in mitochondrial dysfunction, autophagy inhibition, and a significant increase in the rate of apoptosis of NP cells. Meanwhile, mitophagy inhibition enhanced H2O2-induced apoptosis. Furthermore, repression of Parkin significantly attenuated mitophagy and exacerbated apoptosis.ConclusionThese results suggested that Parkin may play a protective role in alleviating the apoptosis of NP cells via mitophagy, and that targeting Parkin may provide a promising therapeutic strategy for the prevention of IDD.

scholarly journals Long Noncoding RNA ANPODRT Overexpression Protects Nucleus Pulposus Cells from Oxidative Stress and Apoptosis by Activating Keap1-Nrf2 Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Liang Kang ◽  
Yueyang Tian ◽  
Xing Guo ◽  
Xu Chu ◽  
Yuan Xue
Keyword(s):  
Oxidative Stress ◽  
Nucleus Pulposus ◽  
Noncoding Rna ◽  
Target Genes ◽  
Nuclear Translocation ◽  
Related Factor ◽  
Nucleus Pulposus Cells ◽  
Tert Butyl Hydroperoxide ◽  
Antioxidative Stress ◽  
Opposing Effects

Oxidative stress and subsequent nucleus pulposus (NP) cell apoptosis are important contributors to the development of intervertebral disc degeneration (IDD). Emerging evidences show that long noncoding RNAs (lncRNAs) play a role in the pathogenesis of IDD. In this study, we investigated the role of lncRNA ANPODRT (anti-NP cell oxidative damage-related transcript) in oxidative stress and apoptosis in human NP cells. We found that ANPODRT was downregulated in degenerative NP tissues and in NP cells treated with tert-butyl hydroperoxide (TBHP, the oxidative stress inducer). ANPODRT overexpression alleviated oxidative stress and apoptosis in NP cells exposed to TBHP, while ANPODRT knockdown exerted opposing effects. Mechanistically, ANPODRT facilitated nuclear factor E2-related factor 2 (Nrf2) accumulation and nuclear translocation and activated its target genes by disrupting the kelch-like ECH-associated protein 1- (Keap1-) Nrf2 association in NP cells. Nrf2 knockdown abolished the antioxidative stress and antiapoptotic effects of ANPODRT in NP cells treated with TBHP. Collectively, our findings suggest that ANPODRT protects NP cells from oxidative stress and apoptosis, at least partially, by activating Nrf2 signaling, implying that ANPODRT may be a potential therapeutic target for IDD.

scholarly journals The REDD1/TXNIP Complex Accelerates Oxidative Stress-Induced Apoptosis of Nucleus Pulposus Cells through the Mitochondrial Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-22
Author(s):  
Huipeng Yin ◽  
Kun Wang ◽  
Abhirup Das ◽  
Gaocai Li ◽  
Yu Song ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intervertebral Disc ◽  
Nucleus Pulposus ◽  
Cell Apoptosis ◽  
Redox Homeostasis ◽  
Mitochondrial Pathway ◽  
Nucleus Pulposus Cells ◽  
Damage Response ◽  
Induced Apoptosis ◽  
Ivd Degeneration

The death of nucleus pulposus (NP) cells is an important cause of intervertebral disc (IVD) degeneration. Redox disturbance caused by dysfunctional mitochondria has been considered as a vital risk for NP cell survival. It is valuable to identify key proteins maintaining mitochondrial function in NP cells. A previous study found that regulated in development and DNA damage response 1 (REDD1) are upregulated during intervertebral disc degeneration and that REDD1 can cause NP cell apoptosis. Thus, the present study further explores the effect of REDD1 on IVD degeneration. Our results showed that REDD1 promotes NP cell apoptosis via the mitochondrial pathway. Importantly, REDD1 formed a complex with TXNIP to strengthen its own action, and the combination was consolidated under H2O2-induced oxidative stress. The combined inhibition of the REDD1/TXNIP complex was better than that of REDD1 or TXNIP alone in restoring cell proliferation and accelerating apoptosis. Moreover, p53 acts as the transcription factor of REDD1 to regulate the REDD1/TXNIP complex under oxidative stress. Altogether, our results demonstrated that the REDD1/TXNIP complex mediated H2O2-induced human NP cell apoptosis and IVD degeneration through the mitochondrial pathway. Interferences on these sites to achieve mitochondrial redox homeostasis may be a novel therapeutic strategy for oxidative stress-associated IVD degeneration.

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