Abstract
The current study evaluated the effects of taxifolin treatments on the viability of osteoblast-like cells, and on the expression of early mineralization markers, as part of the ongoing search for new endodontic materials able to induce periapical healing without causing cytotoxicity. Saos-2 osteoblast-like cells were exposed to different concentrations of taxifolin (5 and 10 µM), applied as pretreatments either for 24h and 72h, or continuously throughout the experimental protocol. Cell viability using the methylthiazole tetrazolium (MTT) assay, alkaline phosphatase activity using thymolphthalein monophosphate assays, deposition of mineralized nodules using alizarin red staining, and expression of ALP and COL-1 by qPCR were determined after 6 and 13 days of treatment. The data were analyzed statistically (p<0.05). Taxifolin was not cytotoxic in the concentrations tested. Pretreatments with taxifolin for 24h and 72h at 10 µM stimulated ALP activity, and increased mineralized nodule deposition by Saos-2 cells. Continuous treatment with taxifolin was not effective in stimulating ALP activity and mineralization. ALP and COL-1 gene expression increased with taxifolin pretreatments, since the highest mRNA levels were observed after 72h of pretreatment with taxifolin at 10 µM on day 13. In conclusion, taxifolin was cytocompatible, and induced mineralization markers when applied for short periods in osteoblast-like cell culture.
Highlights
Bone formation is a complex process which involves different cell types, such as proliferating pre-osteoblasts, bone matrix-producing osteoblasts, osteocytes, and osteoclasts, which are responsible for bone reabsorption and remodeling
In an effort to further the ongoing search for new endodontic materials able to induce periapical healing without causing cytotoxicity,[16,17] the present study aimed to evaluate the effects of taxifolin treatments on the viability of a human osteoblast-like cell line (Saos-2) and the expression of mineralization markers
No statistical differences were observed between the pretreatments and continuous treatments, except for T10-CT at 6 and 13 days
Summary
Bone formation is a complex process which involves different cell types, such as proliferating pre-osteoblasts, bone matrix-producing osteoblasts, osteocytes (or mature bone-lining cells), and osteoclasts, which are responsible for bone reabsorption and remodeling. The events of bone formation are modulated by several hormones and cell products secreted in response to tissue injury.[1,2] In vitro models of osteogenesis and bone nodule formation have been used to assess the effects of new compounds on the proliferation, differentiation, and mineralized matrix deposition of osteoblastic cells.[3] A substantial number of genes, including alkaline phosphatase (ALP), type I collagen (COL-1), bone morphogenetic protein-2 (BMP-2), and osteocalcin (OCN) are highly. Osteoblasts begin mineral deposition, which extends along and within the collagen fibrils.[2,4]
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