ArticleMolecular and cellular biochemistry2026
In vitro evaluation of hydroxyapatite, β-tricalcium phosphate, graphene oxide and zinc oxide for osteochondral regeneration under inflammatory conditions.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The repair of osteochondral defects is challenging due to differing regenerative capacities of bone and cartilage, a challenge that is often exacerbated by chronic inflammation. This study evaluated the immunomodulatory and regenerative potential of hydroxyapatite (HAp), β-tricalcium phosphate (β-TCP), graphene oxide (GO), and zinc oxide (ZnO) on osteoblast-like cells (Saos-2) and chondrocyte-like cells (SW1353) under IL-1β-induced inflammatory conditions. An MTT assay was used to measure cell viability at different concentrations of substances. To investigate the ability of Saos-2 cells to synthesize an inorganic extracellular matrix (ECM), mineralisation was observed via Alizarin Red staining and alkaline phosphatase (ALP) activity. The protein production of pro-COL1, pro-COL2, ACAN, MMP-9, IL-6, IL-8, BMP-2/4, RUNX2, and SOX9 was assessed using ELISA and Western blotting. The gene expression of RUNX2, SOX9, MMP-3, ADAMTS-5, COL10A1, ACAN, BGLAP, and FGF-2 was evaluated using RT-qPCR. Under inflammatory conditions, all the evaluated substances maintained basal matrix synthesis while suppressing the expression of ECM-degrading enzymes. Notably, GO exhibited a strong chondroprotective effect in SW1353 cells by significantly downregulating the expression of RUNX2 and FGF-2. Conversely, ZnO was found to impair mineralisation via the cytoplasmic trapping of RUNX2. Furthermore, their distinct impact on cellular phenotypes, ranging from GO-mediated chondroprotection to the inhibition of mineralisation by ZnO, highlights that the strategic, layer-specific integration of these substances is essential for actively guiding and sustaining the complex process of osteochondral healing. Consequently, our findings demonstrate a dual therapeutic benefit, in which the evaluated substances simultaneously suppress ECM degradation and support fundamental matrix synthesis under inflammatory stress.
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