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2-O-digalloyl-1,3,4,6-tetra-O-galloyl-モ-D-glucose isolated from Galla Rhois suppresses osteoclast differentiation and function by inhibiting NF-リB signaling
Hye Jung Ihn1,#, Tae Hoon Kim2,#, Kiryeong Kim3, Gi-Young Kim4, You-Jin Jeon4, Yung Hyun Choi5, Jong-Sup Bae6, Jung-Eun Kim7, Eui Kyun Park3,*
1Institute for Hard Tissue and Bio-tooth Regeneration (IHBR), Kyungpook National University,
2Department of Food Science and Biotechnology, Daegu University,
3Department of Oral Pathology and Regenerative Medicine, School of Dentistry, IHBR, Kyungpook National University,
4Department of Marine Life Sciences, School of Marine Biomedical Sciences, Jeju National University,
5Department of Biochemistry, College of Korean Medicine, Dong-Eui University,
6College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences and 7Department of Molecular Medicine, School of Medicine, Kyungpook National University
Natural compounds isolated from medicinal herbs and plants have immense significance in maintaining bone health. Hydrolysable tannins have been shown to possess a variety of medicinal properties including antiviral, anticancer, and anti-osteoclastogenic activities. As a part of a study on the discovery of alternative agent against skeletal diseases, we isolated a hydrolysable tannin, 2-O-digalloyl-1,3,4,6-tetra-O-galloyl-モ-D-glucose (DTOGG), from Galla Rhois and examined the effect on osteoclast formation and function. We found that DTOGG significantly inhibited receptor activator of nuclear factor-リB ligand (RANKL)-induced osteoclast differentiation by downregulating the expression of the key regulator in osteoclastogenesis as well as osteoclast-related genes. Analysis of RANKL/RANK signaling revealed that DTOGG impaired activation of IリBメ and p65 in the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-リB) signaling pathway. Furthermore, DTOGG reduced bone resorbing activity of osteoclasts, compared to the vehicle-treated control. These results suggest that DTOGG could be a useful natural compound to manage osteoclast-mediated skeletal diseases.
Abstract, Accepted Manuscript [Submitted on March 5, 2019, Accepted on April 25, 2019]
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