Combination of baicalein and miR‑106a‑5p mimics significantly alleviates IL‑1β‑induced inflammatory injury in CHON‑001 cells

Abstract

Osteoarthritis (OA) induces inflammation and degeneration of all joint components, and as such, is a consid- erable 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)-1beta. 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-alpha in the cell culture medium were quan- tified via ELISA. The present study revealed that treatment with BAI or miR-106a-5p mimic alleviated IL-1beta-induced apoptosis, and BAI + miR-106a-5p combination treatment exerted enhanced anti-inflammatory effects compared with monotherapy. Furthermore, IL-1beta-induced accumulation of collagen, collagen III, MMP-13 and MMP-9 in CHON-001 cells was reversed to a greater degree following combina- tion treatment compared with monotherapy. Likewise, IL-1beta-induced aggrecan degradation was markedly reversed by combination treatment. IL-1beta-induced upregulation of active Notch1 and Hes1 in CHON-001 cells was also signifi- cantly 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-1beta-induced inflammatory injury in CHON-001 cells, which may serve as a novel therapeutic strategy for OA.Copyright © This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) License.