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Recent work has shown that nitric oxide (NO) induction by nitricoxide synthase(NOS) is the physiological mediator of bone cell function and demonstrated that it may be possible to exert differential effects on osteoblast (OB) and osteoclast (OC) activity in vivo. The proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interferon-γ (IFN-γ), will stimulate bone resorption by NOS-induced low levels of NO. These findings confirm NO as a potentially important osteoblast-osteoclast coupling factor, indicating that cytokine-induced NO was largely responsible for the mechanisms of osteoporosis. Pharmacological modulation of NO may therefore represent a new approach in the treatment of bone diseases characterized by increased bone resorption, such as osteoporosis (OP).

作者:李昂;萧劲夫;薛延

来源:中国病理生理杂志 2001 年 17卷 2期

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| 浏览:229 | 下载:5
作者:
李昂;萧劲夫;薛延
来源:
中国病理生理杂志 2001 年 17卷 2期
标签:
骨质疏松 一氧化氮 成骨细胞 破骨细胞
Recent work has shown that nitric oxide (NO) induction by nitricoxide synthase(NOS) is the physiological mediator of bone cell function and demonstrated that it may be possible to exert differential effects on osteoblast (OB) and osteoclast (OC) activity in vivo. The proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interferon-γ (IFN-γ), will stimulate bone resorption by NOS-induced low levels of NO. These findings confirm NO as a potentially important osteoblast-osteoclast coupling factor, indicating that cytokine-induced NO was largely responsible for the mechanisms of osteoporosis. Pharmacological modulation of NO may therefore represent a new approach in the treatment of bone diseases characterized by increased bone resorption, such as osteoporosis (OP).