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Combination of baicalein and miR-106a-5p mimics significantly alleviates IL-1β-induced inflammatory injury in CHON-001 cells
Osteoarthritis (OA) induces inflammation and degeneration of all joint components, and as such, is a considerable source of disability, pain and socioeconomic burden worldwide. Baicalein (BAI) and microRNA (miR)-106a-5p suppress the progression of OA; however, the effects of BAI and miR-106a-5p for...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7903477/ https://www.ncbi.nlm.nih.gov/pubmed/33732318 http://dx.doi.org/10.3892/etm.2021.9776 |
Sumario: | Osteoarthritis (OA) induces inflammation and degeneration of all joint components, and as such, is a considerable source of disability, pain and socioeconomic burden worldwide. Baicalein (BAI) and microRNA (miR)-106a-5p suppress the progression of OA; however, the effects of BAI and miR-106a-5p for the combined treatment of OA are not completely understood. An in vitro OA model was established by treating CHON-001 cells with 20 ng/ml interleukin (IL)-1β. Cell Counting Kit-8 and flow cytometry assays were conducted to evaluate cell viability and apoptosis, respectively. Western blotting was performed to determine the expression levels of Bax, active caspase-3, Bcl-2, collagen I, collagen III, aggrecan, matrix metallopeptidase (MMP)-13, MMP-9, active Notch1 and transcription factor hes family bHLH transcription factor 1 (Hes1). The levels of IL-6 and tumor necrosis factor-α in the cell culture medium were quantified via ELISA. The present study revealed that treatment with BAI or miR-106a-5p mimic alleviated IL-1β-induced apoptosis, and BAI + miR-106a-5p combination treatment exerted enhanced anti-inflammatory effects compared with monotherapy. Furthermore, IL-1β-induced accumulation of collagen, collagen III, MMP-13 and MMP-9 in CHON-001 cells was reversed to a greater degree following combination treatment compared with monotherapy. Likewise, IL-1β-induced aggrecan degradation was markedly reversed by combination treatment. IL-1β-induced upregulation of active Notch1 and Hes1 in CHON-001 cells was also significantly attenuated by combined BAI + miR-106a-5p treatment. In conclusion, the results of the present study revealed that the combination of BAI and miR-106a-5p mimic significantly decreased IL-1β-induced inflammatory injury in CHON-001 cells, which may serve as a novel therapeutic strategy for OA. |
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