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Acer tegmentosum Maxim Prevents Bone Loss by Inhibiting Osteoclastogenesis and Promoting Osteoblast Mineralization in Ovariectomized Mice

  • Oh, Tae Woo (Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM)) ;
  • Park, Kwang-Il (Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM)) ;
  • Do, Hyun Ju (Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM)) ;
  • Kim, Kyungho (Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM)) ;
  • Yang, Hye Jin (Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM)) ;
  • Cho, Won Kyung (Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM)) ;
  • Ma, Jin Yeul (Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM))
  • 투고 : 2019.12.05
  • 심사 : 2020.03.11
  • 발행 : 2020.03.31

초록

Osteoporosis is a worldwide disease leading to significant economic and societal burdens globally. Osteoporosis is caused by unbalanced bone remodeling between the rate of osteoclast bone resorption and osteoblast bone formation. Acer tegmentosum Maxim (AT) is a traditional herbal medicine containing multiple biological activities such as anti-oxidant and anti-inflammatory purposes. However, its role in osteoporosis has not been fully studied. Therefore, we investigated whether AT has a potent inhibitory effect on osteoporosis and its mechanism through a systemic evaluation in ovariectomized (OVX) mice. OVX mice were orally administrated with the AT at doses of 50, 100, and 200 mg/kg for 10 weeks. Histological images and histomorphometry analyses were performed by H&E and Toluidine blue satin, and the expression levels of receptor activator for nuclear factor-kB ligand (RANKL), nuclear factor of activated T cells cytoplasm 1 (NFATc1), c-Fos, and matrix metalloproteinase 9 (MMP9) related to the osteoclast differentiation were investigated using immunohistochemical analysis. Administration of AT prevented bone loss and the alternations of osteoporotic bone parameters at the distinct regions of the distal femur and spongiosa region in OVX mice. Further, administration of AT increased periosteal bone formation in a dose-dependent manner. Meanwhile, AT inhibited not only the expression of NFATc1 and c-Fos, which are two major regulators of osteoclastogenesis but also reduced bone resorbed encoding expression of MMP9 and RANKL. Our results indicated that administration of AT prevented bone loss and the alternations of osteoporotic bone parameters at the distinct regions of the distal femur and spongiosa region in OVX mice. Also AT has the bone protective effect through the suppression of osteoclast and promotion of osteoblast, suggesting that it could be a preventive and therapeutic candidate for anti-osteoporosis.

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