International Journal of Pharmacology

Volume 17 (8), 621-633, 2021


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Nanosize Hydroxyapatite Significantly Repairs the Bone Damage Caused by Several Genes

Yang Liu, Hao Liu and Chengli Liu

Background and Objective: Hydroxyapatite (HA) is a naturally occurring mineral type of calcium apatite, calcium, phosphorus and oxygen. Which makes up most of the bone structure of humans, forms tooth enamel and presents in small amounts in the brain. The purpose of this study was to synthesize nano-sized hydroxyapatite particles as a synthetic medicine for the gene mutations which cause bone damage. Materials and Methods: For this purpose, an aqueous solution of calcium nitrate tetrahydrate and diammonium hydrogen phosphate at pH 10 was used. Furthermore, molecular docking was performed to determine the interactions of HA with several mutated genes (BMP2, COL1A, IGF-1, PDGF and TGF-β) which are responsible for bone damage to determine its efficacy as a therapy against these mutated genes. Results: HA size was ranging from 100-200 nm, after synthesis, HA did not decompose into any other step, even after 1 hr of air heating at 1000°C, which confirmed its stability. In all the docked complexes, lower binding energies (-7.088 to -11.673 kcal mol–1) and positive binding efficiencies, 0.79-0.89 kcal mol–1 were obtained which validated molecular docking results. Both the synthesis and the molecular docking results indicated that HA is a better binding agent to correct bone damage and can be used as a bone implant. Conclusion: HA is a potent inhibitor of mutated bone healing genes (BMP2, COL1A, IGF-1, PDGF and TGF-β). In the future, this work can be further accessed in clinical trials to determine the efficacy of HA against the above-listed gene mutations.

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How to cite this article:

Yang Liu, Hao Liu and Chengli Liu, 2021. Nanosize Hydroxyapatite Significantly Repairs the Bone Damage Caused by Several Genes. International Journal of Pharmacology, 17: 621-633.


DOI: 10.3923/ijp.2021.621.633
URL: https://ansinet.com/abstract.php?doi=ijp.2021.621.633

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