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Puerarin Prevents LPS-Induced Osteoclast Formation and Bone Loss via Inhibition of Akt Activation  ( SCI-EXPANDED收录)   被引量:37

文献类型:期刊文献

英文题名:Puerarin Prevents LPS-Induced Osteoclast Formation and Bone Loss via Inhibition of Akt Activation

作者:Zhang, Yun[1];Yan, Ming[2];Yu, Qing-feng[1];Yang, Pei-fan[1];Zhang, Hai-dong[1];Sun, Yong-hong[3];Zhang, Zhi-fen[1];Gao, Yun-feng[1]

机构:[1]Shaoxing Univ, Coll Med, Huancheng West Rd 508, Shaoxing 312000, Peoples R China;[2]Hangzhou Dianzi Univ, Coll Life Informat Sci & Instrument Engn, Dept Biomed Engn, 2nd Ave 1158, Hangzhou 310018, Zhejiang, Peoples R China;[3]Zhejiang Univ, Dept Biomed Engn, Zhejiang Prov Key Lab Cardiocerebral Vasc Detect, Hangzhou 310027, Zhejiang, Peoples R China

年份:2016

卷号:39

期号:12

起止页码:2028

外文期刊名:BIOLOGICAL & PHARMACEUTICAL BULLETIN

收录:SCI-EXPANDED(收录号:WOS:000389014700016)、、Scopus(收录号:2-s2.0-85006109879)、WOS

基金:This work was supported by Zhejiang Provincial Natural Science Foundation of China (LY17H060007, LY15H180012 and LY13H060003), National Natural Science Foundation of China (30900301), Applied Research Program of Public Good in Zhejiang Province (2011C33046) and Scientific Research Foundation of Traditional Chinese Medicine in Zhejiang Province (2012ZB161).

语种:英文

外文关键词:puerarin; lipopolysaccharide (LPS); osteoclastogenesis; bone loss; Akt

外文摘要:Osteolysis induced by chronic Gram-negative bacterial infection underlies many bone diseases such as osteomyelitis, septic arthritis, and periodontitis. Drugs that inhibit lipopolysaccharide (LPS)-induced osteolysis are critically needed for the prevention of bone destruction in infective bone diseases. In this study, we assessed the effect of puerarin, a natural isoflavone isolated from Pueraria lobata OHWI root, on LPS-induced osteoclastogenesis and bone loss. Our in vitro study showed that puerarin significantly inhibited LPS-induced osteoclast differentiation from osteoclast precursor RAW264.7 cells. The inhibition occurred through suppressing the production of osteoclast activating factor tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta and prostaglandin E-2 (PGE(2)), which led to down-regulating mRNA expression of osteoclastogenic genes including tartrate-resistant acid phosphatase (TRAP), cathepsin K and matrix metalloprotein 9 (MMP-9). Furthermore, LPS triggered activation of Akt in osteoclast precursor RAW264.7 cells, which was inhibited by puerarin treatment. In vivo, puerarin attenuated LPS-induced bone loss in a murine calvarial osteolysis model. Collectively, puerarin prevents LPS-induced osteoclast formation, function and bone loss, where the inhibition of Akt activation plays an important role. These findings provide evidences that puerarin might be beneficial as a promising candidate drug for the prevention and treatment of bacteria-induced bone destruction disease, and give new insights for understanding its possible mechanism.

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