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Arch Gerontol Geriatr ; 102: 104748, 2022.
Article in English | MEDLINE | ID: mdl-35704952

ABSTRACT

PURPOSE: Intervertebral disc degeneration is an abnormal, cell-mediated process of tissue remodeling, recognized as the principal cause of low back pain affecting 80% of the population worldwide. Inflammatory cytokine, Interleukin-1beta (IL-1ß) is involved in the intervertebral disc degeneration (IDD) process, and it is upregulated in degenerated discs. Omentin-1, also known as intelectin-1, is an adipokine with anti-inflammatory, anti-apoptosis, pro-proliferation, and proangiogenic properties in various types of cells. However, little is known about the effects of omentin-1 on human nucleus pulposus cells (HNPCs). This study aims to investigate the effects of omentin-1 on healthy HNPCs regarding proliferation and further investigate the effects of omentin-1 on IL-1ß-induced inflammation, apoptosis, and degeneration in HNPCs. METHODS: Genes and proteins of interest were measured by qRT-PCR, immunoblotting, and immunofluorescence to conduct related experiments. Cell viability (CCK-8), EdU, and mitochondrial membrane potential (JC-1), flow cytometry assays were used to assess proliferation and apoptosis, respectively. RESULTS: Our study showed that omentin-1 promoted proliferation in normal HNPCs. Furthermore, omentin-1 expression was decreased in IL-1ß-treated HNPCs. Omentin-1 protected against IL-1ß-induced inflammation, apoptosis, and degeneration in HNPCs in vitro via the activation of the PI3K/Akt signaling pathway. CONCLUSION: These findings may contribute to understanding the role of omentin-1 in HNPCs and may be a potential therapeutic candidate for intervertebral disc degeneration.


Subject(s)
Cytokines , Intervertebral Disc Degeneration , Lectins , Nucleus Pulposus , Cell Proliferation , Cytokines/genetics , Cytokines/metabolism , GPI-Linked Proteins/genetics , GPI-Linked Proteins/metabolism , Humans , Inflammation/metabolism , Intervertebral Disc Degeneration/genetics , Intervertebral Disc Degeneration/metabolism , Lectins/genetics , Lectins/metabolism , Nucleus Pulposus/metabolism , Phosphatidylinositol 3-Kinases/metabolism
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