Dihydromyricetin Protects against Bone Loss in Ovariectomized Mice by Suppressing Osteoclast Activity.
Dihydromyricetin Protects against Bone Loss in Ovariectomized Mice by Suppressing Osteoclast Activity.
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二氢杨梅素通过抑制破骨细胞活性来防止卵巢切除小鼠的骨质流失
DOI：
10.3389/fphar.2017.00928
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发表时间：
2017
影响因子：
5.6
通讯作者：
Xiao J
中科院分区：
文献类型：
--
作者：
Zhao L;Cai C;Wang J;Zhao L;Li W;Liu C;Guan H;Zhu Y;Xiao J
二氢杨梅素(DMY)是显齿蛇葡萄中的主要黄酮类成分，具有治疗炎症和氧化损伤相关疾病的药理活性。由于破骨细胞经常参与慢性低度全身炎症和氧化损伤，我们推测DMY可能是治疗破骨细胞相关疾病的有效方法。体外观察DMY对破骨细胞形成和活性的影响。将雌性C57BL/6小鼠摘除卵巢，模拟绝经后骨丢失，给予DMY治疗，取股骨标本进行骨结构和组织学分析，并测定血清生化指标。DMY可抑制核因子-κB、c-Fos和丝裂原活化蛋白激酶的激活，并阻止活性氧的产生。DMY降低破骨细胞特异性基因的表达，包括Trap、MMP-9、组织蛋白酶K、C-Fos、NFATc1和Rank。此外，DMY还可防止骨丢失，降低血清肿瘤坏死因子-α、白介素1β和白介素6水平，降低体内核因子受体激活剂RANK配体(RANKL)与骨保护素(OPG)的比值。这些发现表明，DMY通过调节RANKL信号的上下游多条途径，减轻骨丢失，抑制破骨细胞的形成和活性。因此，DMY可能是治疗破骨细胞相关疾病，如类风湿性关节炎和骨质疏松症的有用选择。
Dihydromyricetin (DMY), the main flavonoid component of Ampelopsis grossedentata, possesses pharmacological activities useful for treatment of diseases associated with inflammation and oxidative damage. Because osteoclasts are often involved in chronic low-grade systemic inflammation and oxidative damage, we hypothesized that DMY may be an effective treatment for osteoclast-related diseases. The effects of DMY on osteoclast formation and activity were examined in vitro. Female C57BL/6 mice were ovariectomized to mimic menopause-induced bone loss and treated with DMY, and femur samples were subjected to bone structure and histological analysis, serum biochemical indicators were also measured. DMY suppressed the activation of nuclear factor-κB, c-Fos and mitogen-activated protein kinase, and prevented production of reactive oxygen species. DMY decreased expression of osteoclast-specific genes, including Trap, Mmp-9, Cathepsin K, C-Fos, Nfatc1, and Rank. In addition, DMY prevented bone loss and decreased serum levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6, and with a decrease in the ratio between receptor activator of nuclear factor-κB (RANK) ligand (RANKL) and osteoprotegerin (OPG) in vivo. These findings demonstrate that DMY attenuates bone loss and inhibits osteoclast formation and activity through modulation of multiple pathways both upstream and downstream of RANKL signaling. DMY may thus be a useful option for treatment of osteoclast-related diseases such as rheumatoid arthritis and osteoporosis.
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影响因子：
2.6
作者：
Shen, Chwan-Li;Chyu, Ming-Chien
通讯作者：
Chyu, Ming-Chien
影响因子：
5.1
作者：
Hou, X. L.;Tong, Q.;Fang, J. G.
通讯作者：
Fang, J. G.
影响因子：
--
作者：
Chen Y;Lv L;Pi H;Qin W;Chen J;Guo D;Lin J;Chi X;Jiang Z;Yang H;Jiang Y
通讯作者：
Jiang Y
糖皮质激素：通过活性氧和自噬对破骨细胞形成和功能产生剂量相关的影响。
影响因子：
4.1
作者：
Shi, Jun;Wang, Long;Luo, Zhuojing
通讯作者：
Luo, Zhuojing
环氧类二十烷酸抑制破骨细胞生成并防止卵巢切除术引起的骨质流失。
影响因子：
4.8
作者：
Guan, Hanfeng;Zhao, Libo;Xiao, Jun
通讯作者：
Xiao, Jun