Naringin Protects Against Interleukin 1β (IL-1β)-Induced Human Nucleus Pulposus Cells Degeneration via Downregulation Nuclear Factor kappa B (NF-κB) Pathway and p53 Expression

Aims Inflammatory response plays a pivotal role in the pathophysiological process of intervertebral disc degeneration (IDD). A20 (also known as tumour necrosis factor alpha-induced protein 3 (TNFAIP3)) is a ubiquitin-editing enzyme that restricts nuclear factor-kappa B (NF-κB) signalling. A20 prevents the occurrence of multiple inflammatory diseases. However, the role of A20 in the initiation of IDD has not been elucidated. The aim of the study was to investigate the effect of A20 in senescence of TNF alpha (TNF-α)-induced nucleus pulposus cells (NPCs). Methods Immunohistochemical staining was performed to observe the expression of A20 in normal and degenerated human intervertebral discs. The NPCs were dissected from the tail vertebrae of healthy male Sprague-Dawley rats and were cultured in the incubator. In the experiment, TNF-α was used to mimic the inflammatory environment of IDD. The cell viability and senescence were examined to investigate the effect of A20 on TNF-α-treated NPCs. The expression of messenger RNA (mRNA)-encoding proteins related to matrix macromolecules (collagen II, aggrecan) and senescence markers (p53, p16). Additionally, NF-κB/p65 activity of NPCs was detected within different test compounds. Results The expression of A20 was upregulated in degenerate human intervertebral discs. The A20 levels of NPCs in TNF-α inflammatory microenvironments were dramatically higher than those of the control group. TNF-α significantly decreased cell proliferation potency but increased senescence-associated beta-galactosidase (SA-β-Gal) activity, the expression of senescence-associated proteins, the synthesis of extracellular matrix, and G1 cycle arrest. The senescence indicators and NF-κB/p65 expression of A20 downregulated group treated with TNF-α were significantly upregulated compared to TNF-α-treated normal NPCs. Conclusion A20 has a self-protective effect on the senescence of NPCs induced by TNF-α. The downregulation of A20 in NPCs exacerbated the senescence of NPCs induced by TNF-α. Cite this article: Bone Joint Res. 2020;9(5):225–235.

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Shikonin protects against lipopolysaccharide‐induced inflammation and apoptosis in human nucleus pulposus cells through the nuclear factor‐kappa B pathway

Food Science & Nutrition ◽

10.1002/fsn3.2519 ◽

2021 ◽

Author(s):

Yuanbin Liu ◽

Jiazhuang Zheng ◽

Yu Chen ◽

Fandong Wang ◽

He Ye ◽

...

Keyword(s):

Nucleus Pulposus ◽

Nuclear Factor Kappa B ◽

Nuclear Factor ◽

Nucleus Pulposus Cells ◽

Nuclear Factor Kappa

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Effect of a Cyclooxygenase-2 Inhibitor on Interleukin-1β–Stimulated Activation of the Transcription Factor Nuclear Factor-Kappa B in Human Gingival Fibroblasts

Journal of Periodontology ◽

10.1902/jop.2007.060250 ◽

2007 ◽

Vol 78 (3) ◽

pp. 542-549 ◽

Cited By ~ 9

Author(s):

David A. Tipton ◽

Denise C. Gay ◽

Vaughn A. DeCoster

Keyword(s):

Transcription Factor ◽

Nuclear Factor Kappa B ◽

Cyclooxygenase 2 ◽

Human Gingival Fibroblasts ◽

Interleukin 1Β ◽

Nuclear Factor ◽

Gingival Fibroblasts ◽

Nuclear Factor Kappa ◽

Transcription Factor Nuclear Factor

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Dihydromyricetin Prevents Inflammation and Oxidative Stress in Human Osteoarthritis Chondrocytes

Current Topics in Nutraceutical Research ◽

10.37290/ctnr2641-452x.20:207-212 ◽

2021 ◽

Vol 20 (1) ◽

pp. 207-212

Author(s):

Pengbo Yao ◽

Jinwei Ai

Keyword(s):

Oxidative Stress ◽

Nuclear Factor Kappa B ◽

Therapeutic Potential ◽

Cell Model ◽

Cartilage Degradation ◽

Cartilage Destruction ◽

Interleukin 1Β ◽

Nuclear Factor ◽

Nuclear Factor Kappa

Osteoarthritis is characterized by inflammation and joint cartilage degradation. Dihydromyricetin, a natural flavonoid in rattan tea, exhibits several pharmacological properties including antitumor, cardioprotection, antidiabetes, neuroprotection, hepatoprotection, and dermatoprotection. Herein, we have investigated in vitro the effects of dihydromyricetin on osteoarthritis progression using an interleukin-1β-induced cell model. Our data show that dihydromyricetin markedly improved the viability of interleukin-1β-treated chondrocytes. Furthermore, dihydromyricetin markedly downregulated the expression of nitric oxide, prostaglandin-E2, tumor necrosis factor-α, and interleukin-6, and ameliorated cartilage destruction in interleukin- 1β-treated chondrocytes, as well as inhibited the interleukin-1β-induced oxidative stress via the nuclear factor kappa B axis. In summary, our results demonstrate therapeutic potential of dihydromyricetin in osteoarthritis through modulation of the nuclear factor kappa B signaling pathway.

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