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  • 醫學英文摘要翻譯

    a b s t r a c t

    Osteoclasts play a crucial role in bone resorption. Since osteoclast differentiation/activation

    is involved in orthodontic tooth movement at the compression sites, the investigation on

    osteoclasts is very important to the field of orthodontics. It is well known that estrogen has

    the protective effect on bone. However, the mechanisms by which estrogen prevents bone

    loss remain to be elucidated. Although estrogen was recently reported to induce apoptosis of

    osteoclasts, the precise mechanisms of estrogen-induced osteoclast apoptosis remained

    controversial with regard to whether estrogen affects osteoclasts directly or not. Here we

    investigated whether estrogen directly induces differentiation and apoptosis of osteoclasts

    in vitro using mouse monocytic RAW264 cells differentiated into osteoclasts by RANKL. It

    was observed that estrogen inhibited RANKL-induced osteoclast differentiation of RAW264

    cells in a dose-dependent manner. Estrogen suppressed p38 phosphorylation while it

    enhanced ERK phosphorylation induced by RANKL, suggesting that modulation of MAPK

    signaling may be involved in inhibition of osteoclast differentiation by estrogen. Next, it was

    shown that estrogen dose-dependently augmented caspase-3 activation in osteoclasts

    differentiated from RAW264 cells by RANKL, demonstrating that estrogen directly enhanced

    apoptosis of osteoclasts. Estrogen-induced caspase-3 activation was attenuated by ICI

    182,780, suggesting that the effects of estrogen on osteoclast apoptosis is mediated through

    estrogen receptors. Thus, these results suggest that estrogen may directly inhibit differentiation

    and induce apoptosis of osteoclasts.

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