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RETRACTED: (2R,3R)Dihydromyricetin inhibits osteoclastogenesis and bone loss through scavenging LPS‐induced oxidative stress and NF‐κB and MAPKs pathways activating
Author(s) -
Zhang Xuejun,
Li Xin,
Fang Jianguo,
Hou Xiaolong,
Fang Huang,
Guo Fengjing,
Li Feng,
Chen Anmin,
Huang Shilong
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27154
Subject(s) - oxidative stress , chemistry , microbiology and biotechnology , scavenging , nf κb , signal transduction , biochemistry , biology , antioxidant
Osteolysis is a serious complication of several chronic inflammatory diseases and is closely associated with a local chronic inflammatory reaction with a variety of causes. However, similarities exist in the mechanisms of their pathological processes. Inflammatory factors and oxidative stress–induced nuclear factor κB (NF‐κB) and mitogen‐activated protein kinases (MAPKs) signaling pathways play a center role in bone erosion. Dihydromyricetin (DMY) is a natural compound with anti‐inflammatory and antioxidative effect, which are commonly used in chronic pharyngitis and alcohol use disorders. In the current study, we identified that DMY attenuated lipopolysaccharide (LPS)–induced oxidative stress through inhibiting the production of reactive oxygen species (ROS) and nitric oxide (NO), downregulated COX‐2 and iNOS, and promoted the activity of the antioxidative system by activating superoxide dismutase (SOD) and Nrf2/HO‐1 pathway. To further investigate the underlying mechanism, we found that DMY inhibits osteoclast (OC) differentiation and bone resorption activity through blocking the RANKL‐induced activation of the NF‐κB and MAPKs signaling pathways and then downregulated c‐Fos and NFATc1, which is essential for OC differentiation. Furthermore, DMY inhibited LPS‐induced osteolysis in vivo. Collectively, these results indicate that DMY might be a promising prophylactic antiosteoclastic/resorptive agent in preventing or treating bone lysis diseases.