Abstract
Myricetin, a naturally occurring flavonoid, was investigated to determine whether it could protect osteoblasts from 2-deoxy- d-ribose induced dysfunction and oxidative damage in the MC3T3-E1 cells. MC3T3-E1 cells were incubated with 2-deoxy- d-ribose and/or myricetin, and markers of osteoblast function and oxidative damage were examined. Compared with control incubation, 2-deoxy- d-ribose significantly ( P < 0.05) inhibited alkaline phosphatase (ALP) activity, collagen content, and calcium deposition at the concentration of 20 mM. Cellular malondialdehyde (MDA), protein carbonyl, and advanced oxidation protein products contents were significantly ( P < 0.05) increased in the presence of 2-deoxy- d-ribose (20 mM). Myricetin significantly ( P < 0.05) increased cell survival, ALP activity, collagen, osteocalcin, osteoprotegerin, and calcium deposition and decreased MDA, protein carbonyl, and advanced oxidation protein products contents of osteoblastic MC3T3-E1 cells in the presence of 20 mM 2-deoxy- d-ribose. These results demonstrate that myricetin attenuates 2-deoxy- d-ribose induced damage, suggesting that myricetin may be a useful dietary supplement for minimizing oxidative injury in diabetes related bone diseases.
Published Version
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