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Review
. 2024 Dec 12:15:1486646.
doi: 10.3389/fphar.2024.1486646. eCollection 2024.

Pharmacology and mechanisms of apigenin in preventing osteoporosis

Sun Lin  1 , Wang Yincang  1 , Du Jiazhe  2 , Xu Xilin  3 , Xiaofeng Zhang  1
Affiliations
Review

Pharmacology and mechanisms of apigenin in preventing osteoporosis

Sun Lin et al. Front Pharmacol. .

Abstract

Osteoporosis (OP) stands as the most prevalent systemic skeletal condition associated with aging. The current clinical management of OP predominantly depends on anti-resorptive and anabolic agents. Nevertheless, prolonged use of some of these medications has been observed to reduce efficacy and elevate adverse effects. Given the necessity for sustained or even lifelong treatment of OP, the identification of drugs that are not only effective but also safe and cost-efficient is of utmost significance. As disease treatment paradigms continue to evolve and recent advancements in OP research come to light, certain plant-derived compounds have emerged, presenting notable benefits in the management of OP. This review primarily explores the pharmacological properties of apigenin and elucidates its therapeutic mechanisms in the context of OP. The insights provided herein aspire to offer a foundation for the judicious use of apigenin in forthcoming research, particularly within the scope of OP.

Keywords: apigenin; inflammatory factors; osteoblasts; osteoporosis; oxidative stress.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
The chemical structure of Apigenin.
FIGURE 2
FIGURE 2
The production process of Apigenin. Biosynthesis process of API.
FIGURE 3
FIGURE 3
Biosynthesis process of API.
See this image and copyright information in PMC

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References

    1. Aibar-Almazán A., Voltes-Martínez A., Castellote-Caballero Y., Afanador- Restrepo D. F., Carcelén-Fraile M. D. C., López-Ruiz E. (2022). Current status of the diagnosis and management of osteoporosis management of osteoporosis. Int. J. Mol. Sci. 23(16):9465. 10.3390/ijms23169465 - DOI - PMC - PubMed
    1. Alfaleh M. A., Hashem A. M., Abujamel T. S., Alhakamy N. A., Kalam M. A., Riadi Y., et al. (2022). Apigenin loaded lipoid-PLGA-TPGS nanoparticles for colon cancer therapy: characterization, sustained release, cytotoxicity, and apoptosis pathways for colon cancer therapy: characterization, sustained release, cytotoxicity, and apoptosis pathways. Polymers 14(17), 3577. 10.3390/polym14173577 - DOI - PMC - PubMed
    1. Ali D., Okla M., Abuelreich S., Vishnubalaji R., Ditzel N., Hamam R., et al. (2024). Apigenin and Rutaecarpine reduce the burden of cellular senescence in bone marrow stromal stem cells. Front. Endocrinol. (Lausanne) 15, 1360054. 10.3389/fendo.2024.1360054 - DOI - PMC - PubMed
    1. An X., Shang F. (2018). RA-XII exerts anti-oxidant and anti-inflammatory activities on lipopolysaccharide-induced acute renal injury by suppressing NF-κB and MAPKs regulated by HO-1/Nrf2 pathway activities on lipopolysaccharide-induced acute renal injury by suppressing NF- κ B and MAPKs regulated by HO-1/Nrf2 pathway. Biochem. Biophys. Res. Commun. 495 (3), 2317–2323. 10.1016/j.bbrc.2017.12.131 - DOI - PubMed
    1. Asadi A., Goudarzi F., Ghanadian M., Mohammadalipour A. (2022). Evaluation of the osteogenic effect of apigenin on human mesenchymal stem cells by inhibiting inflammation through modulation of NF- κ B/I κ B α. Res. Pharm. Sci. 17 (6), 697–706. 10.4103/1735-5362.359436 - DOI - PMC - PubMed

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