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Influence of myricetin on bone health

An osteoblast is a cell that is responsible for bone formation. They produce osteoid, consisting mainly of collagen, and are responsible for mineralization of the osteoid matrix. Osteoblasts arise from osteoprogenitor cells, which are induced to differentiate under the influence of growth factors, such as bone morphogenetic proteins, fibroblast growth factor, platelet-derived growth factor and transforming growth factor beta. Once osteoprogenitors start to differentiate into osteoblasts, they express genetic markers including osterix, Col1, ALP, osteocalcin, osteopontin, and osteonectin. A study at Chia-Nan University of Pharmacy and Science, Taiwan, showed that myricetin induced differentiation and matuaration in cultured human osteoblasts, which was associated with increased bone morphogenetic protein-2 production. They also found that myricetin activated SMAD1/5/8 and p38 mitogen-activated protein kinases. Another study conducted at the same university indicated a potential use of myricetin in preventing osteoporosis [2]. Myricetin acted by inhibiting inflammatory cytokines-mediated apoptosis in osteoblast cells. The survival of osteoblast cells is important in patient with osteoporosis caused by inflamed synovium, such as in rheumatoid arthritis. Myricetin induced a significant induction of differentiation in the human osteoblasts and inhibited anti-Fas IgM-induced apoptosis.

[1] Myricetin induces human osteoblast differentiation through bone morphogenetic protein-2/p38 mitogen-activated protein kinase pathway. Biochem Pharmacol. 2007 Feb 15;73(4):504-14.
[2] Myricetin inhibits the induction of anti-Fas IgM-, tumor necrosis factor-alpha- and interleukin-1beta-mediated apoptosis by Fas pathway inhibition in human osteoblastic cell line MG-63. Life Sci. 2005 Oct 21;77(23):2964-76.

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