Omentin-1 promoted proliferation and ameliorated inflammation, apoptosis, and degeneration in human nucleus pulposus cells

Omentin-1 促进人类髓核细胞增殖并改善炎症、凋亡和退化

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作者:Vladmir Lenine Ferreira Cabral, Feng Wang, Xin Peng, Jiawei Gao, Zhimin Zhou, Rui Sun, Junping Bao, Xiaotao Wu

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.

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.

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-1β) 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-1β-induced inflammation, apoptosis, and degeneration in HNPCs.

Results

Our study showed that omentin-1 promoted proliferation in normal HNPCs. Furthermore, omentin-1 expression was decreased in IL-1β-treated HNPCs. Omentin-1 protected against IL-1β-induced inflammation, apoptosis, and degeneration in HNPCs in vitro via the activation of the PI3K/Akt signaling pathway.

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