&lt;p&gt;Sinapic Acid Inhibits IL-1β-Induced Apoptosis and Catabolism in Nucleus Pulposus Cells and Ameliorates Intervertebral Disk Degeneration&lt;/p&gt;

Huang, Jinfeng; Zheng, Xuan-Qi; Lin, Jialiang; Zhang, Kai; Tian, Haijun; Zhou, Wenxian; Wang, Hui; Gao, Ze; Jin, Haiming; Wu, Ai-Min

doi:10.2147/jir.s278556

Cited by 18 publications

(12 citation statements)

References 51 publications

(57 reference statements)

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“…Subsequently, these pathogenic changes may compromise the integrity of the intervertebral disc, cause abnormal distribution of mechanical load imposed on the spine, and consequently destroy the mechanical properties of the spine. At molecular level, nuclear tor-erythroid 2-related factor-2 (Nrf2) has been reported to process the role of antioxidant and anti-inflammation in many degeneration-related diseases [ 6 ]. Previous studies have demonstrated that activated nuclear factor- (erythroid-derived 2-) like 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway showed inhibitory effect on NF- κ B in NP cells.…”

Section: Introductionmentioning

confidence: 99%

Ulinastatin Ameliorates IL‐1β‐Induced Cell Dysfunction in Human Nucleus Pulposus Cells via Nrf2/NF‐κB Pathway

Luo

Huan

Lin

et al. 2021

Oxidative Medicine and Cellular Longevity

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Low back pain (LBP) has been a wide public health concern worldwide. Among the pathogenic factors, intervertebral disc degeneration (IDD) has been one of the primary contributors to LBP. IDD correlates closely with inflammatory response and oxidative stress, involving a variety of inflammation-related cytokines, such as interleukin 1 beta (IL-1β), which could result in local inflammatory environment. Ulinastatin (UTI) is a kind of acidic protein extracted from human urine, which inhibits the release of tumor necrosis factor alpha (TNF-α) and other inflammatory factors to protect organs from inflammatory damage. However, whether this protective effect of UTI on human nucleus pulposus (NP) exists, and how UTI affects the biological behaviors of human NP cells during IDD remain elusive. In this current study, we revealed that UTI could improve the viability of NP cells and promote the proliferation of NP cells. Additionally, UTI could protect human NP cells via ameliorating IL-1β-induced apoptosis, inflammatory response, oxidative stress, and extracellular matrix (ECM) degradation. Molecular mechanism analysis suggested that the protective effect from UTI on IL-1β-treated NP cells were through activating nuclear factor- (erythroid-derived 2-) like 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway and the suppression of NF-κB signaling pathway. Therefore, UTI may be a promising therapeutic medicine to ameliorate IDD.

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Section: Introductionmentioning

confidence: 99%

Ulinastatin Ameliorates IL‐1β‐Induced Cell Dysfunction in Human Nucleus Pulposus Cells via Nrf2/NF‐κB Pathway

Luo

Huan

Lin

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…It is widely found in various oil crops, grains, vegetables, and berries. SA has anti-inflammatory, antioxidant, and antibacterial effects (Chen, 2016;Huang et al, 2018;Lee, 2018;Huang et al, 2020). It has been proved that SA has a strong effect on reducing the oxidative stress of the liver and colon of rats fed high-fat diet (Yang et al, 2019) and abating the pyroptosis in diabetic atherosclerosis (Han et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Sinapic Acid Reduces Oxidative Stress and Pyroptosis via Inhibition of BRD4 in Alcoholic Liver Disease

et al. 2021

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Alcoholic liver disease (ALD) is one of the main causes of death in chronic liver disease. Oxidative stress and pyroptosis are important factors leading to ALD. Bromodomain-containing protein 4 (BRD4) is a factor that we have confirmed to regulate ALD. As a phenolic acid compound, sinapic acid (SA) has significant effects in antioxidant, anti-inflammatory and liver protection. In this study, we explored whether SA regulates oxidative stress and pyroptosis through BRD4 to play a protective effect in ALD. Male C57BL/6 mice and AML-12 cells were used for experiments. We found that SA treatment largely abolished the up-regulation of BRD4 and key proteins of the canonical pyroptosis signalling in the liver of mice fed with alcohol, while conversely enhanced the antioxidant response. Consistantly, both SA pretreatment and BRD4 knockdown inhibited oxidative stress, pyroptosis, and liver cell damage in vitro. More importantly, the expression levels of BRD4 and pyroptosis indicators increased significantly in ALD patients. Molecule docking analysis revealed a potent binding of SA with BRD4. In conclusion, this study demonstrates that SA reduces ALD through BRD4, which is a valuable lead compound that prevents the ALD process.

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“…As a physiological process, cell apoptosis is a critical type of IDD cell death and is believed to play a vital role in the IDD process [ 24 ]. There is increasing evidence that severely degenerated intervertebral discs are in a state of high oxidative stress that contributes to DNA fragmentation and leads to cell apoptosis [ 36 , 37 ]. Increasing evidence supports the involvement of ERS-initiated cell death in IDD [ 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

The protective effects of dezocine on interleukin-1β-induced inflammation, oxidative stress and apoptosis of human nucleus pulposus cells and the possible mechanisms

et al. 2022

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Intervertebral disc degeneration (IDD) is a natural problem linked to the inflammation. We aimed to investigate the role of dezocine (DEZ) in the development of IDD. Human nucleus pulposus cells (HNPCs) induced by interleukin (IL)-1β was used as a cellular model of IDD. After treatment with DEZ, HNPCs viability was evaluated with a CCK-8 assay. Then, the levels of inflammatory factors, including IL-6 and tumor necrosis factor-α (TNF-α), and oxidative stress-related markers, including reactive oxygen species (ROS), malondialdehyde (MDA) and reduced glutathione (GSH), were tested by RT-qPCR or kits. TUNEL staining was employed to detect cell apoptosis and Western blot was used to determine the expression of proteins related to inflammation, oxidative stress, apoptosis, endoplasmic reticulum stress (ERS) and MAPK signaling. Afterward, PMA, a MAPK signaling pathway agonist, was adopted for exploring the regulatory effects of DEZ on MAPK pathway. Results indicated that DEZ enhanced cell viability of HNPCs after IL-1β exposure. DEZ alleviated the inflammation and oxidative stress, evidenced by decreased levels of IL-6, TNF-α, ROS, MDA, p-NF-κB p65, NF-κB p65 in nucleus, cox-2 and increased levels of NF-κB p65 in cytoplasm, GSH, SOD1 and SOD2. Moreover, DEZ notably inhibited IL-1β-induced apoptosis of HNPCs. Furthermore, DEZ suppressed the levels of ERS-related proteins. The levels of related proteins in MAPK signaling including p-P38 and p-ERK1/2 were remarkably reduced after DEZ administration. By contrast, PMA crippled the impacts of DEZ on inflammation, oxidative stress and apoptosis of HNPCs induced by IL-1β. Collectively, DEZ ameliorates IL-1β-induced HNPCs injury via inhibiting MAPK signaling.

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<p>Sinapic Acid Inhibits IL-1β-Induced Apoptosis and Catabolism in Nucleus Pulposus Cells and Ameliorates Intervertebral Disk Degeneration</p>

Cited by 18 publications

References 51 publications

Ulinastatin Ameliorates IL‐1β‐Induced Cell Dysfunction in Human Nucleus Pulposus Cells via Nrf2/NF‐κB Pathway

Ulinastatin Ameliorates IL‐1β‐Induced Cell Dysfunction in Human Nucleus Pulposus Cells via Nrf2/NF‐κB Pathway

Sinapic Acid Reduces Oxidative Stress and Pyroptosis via Inhibition of BRD4 in Alcoholic Liver Disease

The protective effects of dezocine on interleukin-1β-induced inflammation, oxidative stress and apoptosis of human nucleus pulposus cells and the possible mechanisms

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