期刊
EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY
卷 64, 期 3, 页码 211-216出版社
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.etp.2010.08.008
关键词
Quercitrin; Oxidative stress; Osteoblast differentiation
资金
- National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [20100009222]
The protective effect of quercitrin on the response of osteoblastic MC3T3-E1 cells to oxidative stress was evaluated. Osteoblasts were incubated with H2O2 and/or quercitrin, and markers of osteoblast function and oxidative damage were examined. Quercitrin treatment reversed the cytotoxic effect of H2O2 significantly (P < 0.05). This effect was blocked by ICI182780 and LY294002, suggesting that quercitrin's effect might be involved in estrogen action and results from PI3K mediated signaling pathway. Pretreatment of quercitrin increased collagen content, alkaline phosphatase (ALP) activity, and calcium deposition of osteoblasts compared with H2O2 treated cells and these effects were blocked by ERKs and p33 mitogen-activated protein kinases (MAPKs) inhibitors such as PD98059 and SB203580, respectively. These suggest that quercitrin-induced protective effect against osteoblast dysfunction by oxidative stress is associated with increased activation of ERKs and p38 MAPK. Pretreatment with quercitrin also reduced the increase in bone-resorbing factor, receptor activator of nuclear factor-kB ligand (RANKL) and oxidative damage markers (malondialdehyde, protein carbonyl, and nitrotyrosine) induced by H2O2. These results suggest that quercitrin may be protective against H2O2-induced dysfunction in osteoblasts. (C) 2010 Elsevier GmbH. All rights reserved.
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