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Published:
May 11, 2023DOI:
10.4314/tjpr.v22i4.8Keywords:
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Main Article Content
Long non-coding RNA reprogramming (LncRNA-ROR) attenuate inflammation induced by LPS through the regulation of miRNA-124-3p and inhibition of C5a and TLR4/Myd88/NF-κB pathwaysin C28/12 cells
Abstract
Purpose: Osteoarthritis (OA), inflammation of joint and articular cartilage, is a serious joint disorder and a major cause of pain and disability. LncRNAs exert their role in OA progression. The purpose of this present research is to investigate the impact and molecular mechanism of lncRNA regulator of reprogramming (LncRNA-ROR) on inflammatory damage induced by lipopolysaccharide (LPS) in C28/12 cells.
Methods: The expressions of lncRNA-ROR and miR-124-3p and the mRNA expressions of COX-2, iNOS, IL-8, C5a, and TNF-α were determined in C28/12 cells stimulated with LPS using RT-qPCR. Viability of C28/12 cells was evaluated using CCK-8 assay and C28/12 cell apoptosis was assessed by flow cytometry in LPS-induced C28/12 cells. Moreover, the concentration of IL-8, C5a, and TNF-α and the protein expressions of TLR4/Myd88/NF-κB pathways were examined using Elisa assay.
Results: Results revealed that LPS inhibited the proliferation, enhanced rate of cell apoptosis, and promoted mRNA expressions of iNOS, IL-8, C5a, and TNF-α in C28/12 cells. Besides, the expression of lncRNA-ROR was expressively reduced in C28/12 cells stimulated with LPS and the lncRNA-ROR overexpression markedly reduced the inflammatory injury stimulated by LPS in C28/12 cells. Besides, lncRNA-ROR significantly down-regulated the miR-124-3p expression and miR-124-3p exposure inhibited the protecting impact of lncRNA-ROR on LPS-induced C28/12 cells. Furthermore, lncRNA-ROR suppressed the TLR4/Myd88/NF-κB pathways via suppressing the expression of miR-124-3p in LPS-induced C28/12 cells.
Conclusion: The finding revealed that lncRNA-ROR protected against LPS-stimulated inflammatory injury in C28/12 cells by suppressing TLR4/Myd88/NF-κB pathways via inhibiting miR-124-3p suggested an efficient therapeutic strategy for OA treatment.
