The Molecular Mechanism of Vitamin E as a Bone-Protecting Agent: A Review on Current Evidence

Abstract

Bone remodelling is a tightly-coordinated and lifelong process of replacing old damaged bone with newly-synthesized healthy bone. In the bone remodelling cycle, bone resorption is coupled with bone formation to maintain the bone volume and microarchitecture. This process is a result of communication between bone cells (osteoclasts, osteoblasts, and osteocytes) with paracrine and endocrine regulators, such as cytokines, reactive oxygen species, growth factors, and hormones. The essential signalling pathways responsible for osteoclastic bone resorption and osteoblastic bone formation include the receptor activator of nuclear factor kappa-B (RANK)/receptor activator of nuclear factor kappa-B ligand (RANKL)/osteoprotegerin (OPG), Wnt/β-catenin, and oxidative stress signalling. The imbalance between bone formation and degradation, in favour of resorption, leads to the occurrence of osteoporosis. Intriguingly, vitamin E has been extensively reported for its anti-osteoporotic properties using various male and female animal models. Thus, understanding the underlying cellular and molecular mechanisms contributing to the skeletal action of vitamin E is vital to promote its use as a potential bone-protecting agent. This review aims to summarize the current evidence elucidating the molecular actions of vitamin E in regulating the bone remodelling cycle.

Potential Role of Tocotrienols on Non-Communicable Diseases: A Review of Current Evidence

“…The capability of T3 in modulating inflammation has been extensively explored by researchers. T3 acts as regulator for the expression of pro-and anti-inflammatory mediators including TNF-α, IL-1, IL-2, IL-6, IL-8, IL-10, IL-23, IFN-γ, iNOS, and COX-2 [8,404]. The most implicated signal transduction pathways involved in orchestrating inflammatory response are NF-κB, MAPK, signal transducer and activator of transcription (STAT) and Toll-like receptor (TLR) signaling [8,405].…”

“…T3 acts as regulator for the expression of pro-and anti-inflammatory mediators including TNF-α, IL-1, IL-2, IL-6, IL-8, IL-10, IL-23, IFN-γ, iNOS, and COX-2 [8,404]. The most implicated signal transduction pathways involved in orchestrating inflammatory response are NF-κB, MAPK, signal transducer and activator of transcription (STAT) and Toll-like receptor (TLR) signaling [8,405]. Docking studies showed that αT3 blocks the assess of arachidonic acid to the catalytic site of 12-lipoxygenase, thereby achieving its anti-inflammatory effects [406].…”

“…T3 and TF exists naturally as alpha-(α-), beta-(β-), gamma-(γ-), and delta-(δ-) isomers depending on the position of the side chains on the chromanol ring. Both TF and T3 have been regarded as nutraceuticals with a wide range of biological activities against pathological complications, including dyslipidemia [6], cardiovascular [7], musculoskeletal, rheumatoid diseases [8][9][10][11][12][13], gastric [13], neurodegenerative [14], and metabolic diseases [6,15], as well as cancers [16]. The biological effects of T3 can be contributed by its potent anti-inflammatory, anti-oxidative, anti-tumor, cholesterol-lowering [through inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) activity] activities [8,9,17].…”

Histological evaluation of the ANTIOXIDANT effect of Vitamin E on reversing the negative impact of tartrazine on extraction socket healing. (Randomized controlled trial)

“…Vitamin E is an essential lipid-soluble vitamin that consists of two subgroups: tocopherol and tocotrienol (Wong et al, 2019). Due to presence of tocotrienol, there is an improve in proliferation, differentiation, and mineralization, and reduced apoptosis of osteoblastic cells (Abd Manan, Mohamed, & Shuid, 2012)and (Xu et al, 2018).…”

Osteoporosis: From Molecular Mechanisms to Therapies

“…Molecular-based treatment strategies for osteoporosis including current molecular and genetic opinions on osteoporosis and its medical treatment are reviewed by two research groups [11,12]. Wong and colleagues detail how the molecular actions of vitamin E regulate the bone remodeling cycle [13], while Rossi and colleagues discuss the endocannabinoid/endovanilloid system only in osteoporosis and also in bone cancer treatment [14]. Finally, Chin and colleagues review the evidence on the functional food component, tocotrienol, which they suggest may be used to prevent male osteoporosis [15].…”