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Tocotrienol as a Protecting Agent against Glucocorticoid-Induced Osteoporosis: A Mini Review of Potential Mechanisms. | LitMetric

AI Article Synopsis

  • - Glucocorticoid-induced osteoporosis arises from glucocorticoids causing osteoblast apoptosis and promoting fat cell formation in bones.
  • - Tocotrienol shows promise in protecting bones from glucocorticoid harm by reducing oxidative damage and enhancing bone formation, as observed in various studies.
  • - Preclinical evidence suggests that tocotrienol can improve bone structure and health by activating specific biological pathways in osteoblasts, but further validation through randomized controlled trials is necessary.

Article Abstract

Glucocorticoid-induced osteogenic dysfunction is the main pathologyical mechanism underlying the development of glucocorticoid-induced osteoporosis. Glucocorticoids promote adipogenic differentiation and osteoblast apoptosis through various pathways. Various ongoing studies are exploring the potential of natural products in preventing glucocorticoid-induced osteoporosis. Preclinical studies have consistently shown the bone protective effects of tocotrienol through its antioxidant and anabolic effects. This review aims to summarise the potential mechanisms of tocotrienol in preventing glucocorticoid-induced osteoporosis based on existing in vivo and in vitro evidence. The current literature showed that tocotrienol prevents oxidative damage on osteoblasts exposed to high levels of glucocorticoids. Tocotrienol reduces lipid peroxidation and increases oxidative stress enzyme activities. The reduction in oxidative stress protects the osteoblasts and preserves the bone microstructure and biomechanical strength of glucocorticoid-treated animals. In other animal models, tocotrienol has been shown to activate the Wnt/β-catenin pathway and lower the RANKL/OPG ratio, which are the targets of glucocorticoids. In conclusion, tocotrienol enhances osteogenic differentiation and bone formation in glucocorticoid-treated osteoblasts while improving structural integrity in glucocorticoid-treated rats. This is achieved by preventing oxidative stress and osteoblast apoptosis. However, these preclinical results should be validated in a randomised controlled trial.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9506150PMC
http://dx.doi.org/10.3390/molecules27185862DOI Listing

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