Copyright (c) 2023 Junliang Xu, Wei Ji
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Isofraxidin inhibits the proliferation and differentiation of the osteoblast MC3T3-E1 subclone 14 cell line
Corresponding Author(s) : Wei Ji
Cellular and Molecular Biology,
Vol. 69 No. 15: New discoveries in inflammatory factors
Abstract
Ankylosing spondylitis (AS) is an autoimmune inflammatory disease associated with joint inflammation and destruction. Current treatment modalities alleviate symptoms; however, they cannot cure the disease and are associated with significant side effects. Thus, we aimed to confirm the inhibitory effect of isofraxidin, a herbal extract, on pathological osteogenesis in ankylosing spondylitis to better treat patients affected by the disease. Mouse preosteoblast MC3T3-E1 subclone 14 cells were used in vitro to establish control and isofraxidin intervention groups. Cell viability was then determined using the MTT assay; the expression of osteogenic factors, including Runx2, OSX, collagen I, and ALP was measured using qRT-PCR and western blotting. Final osteogenic mineralization was performed by alizarin red staining. The results showed that isofraxidin could inhibit osteoblast viability; however, this effect was nullified at concentrations of 0-20 µM after adding 1% serum. Gene and protein expression of the osteogenic factors RUNX2, OSX, Collagen I, and ALP was inhibited, and a similar trend was exhibited at 7, 14, and 21 days after isofraxidin treatment. This trend was further verified by alizarin red staining of the final osteogenic mineralized nodules on days 7, 14, 21, and 35. Isofraxidin inhibits MC3T3-E1 subclone 14 proliferation and differentiation and may be considered a potential drug therapy for treating pathological osteogenesis in ankylosing spondylitis.
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