Bavachin counteracts receptor activator of nuclear factor-κB-induced osteoclastogenesis though the suppression of nuclear factor-κB signaling pathway in RAW264.7 cells
김복희, 조인아, 강경록, 이숙영, 정서윤, 김재성, 김수관,
소속 상세정보
김복희 ( Kim Bok-Hee ) - Chosun University Institute of Dental Science
조인아 ( Cho In-A ) - Chosun University Institute of Dental Science
강경록 ( Kang Kyeong-Rok ) - Chosun University Institute of Dental Science
이숙영 ( Lee Sook-Young ) - Chosun University Institute of Dental Science
정서윤 ( Jung Seo-Yun ) - Chosun University Institute of Dental Science
김재성 ( Kim Jae-Sung ) - Chosun University Institute of Dental Science
김수관 ( Kim Su-Gwan ) - Chosun University Institute of Dental Science
Abstract
The aim of this study was to evaluate the biological effects and cellular signaling pathways associated with the anti-osteoclastogenesis effects of bavachin, a phytoestrogen, in the receptor activator of nuclear factor-κB ligand (RANKL)- treated RAW264.7 cells. The cell viability of RAW264.7 cells was not affected upon treatment with 5-20 μM bavachin. Furthermore, osteoclastogenesis was suppressed by bavachin in a dose-dependent manner in RAW264.7 cells treated with RANKL. Tartrate-resistant acid phosphatase, matrix metalloproteinase-9, and cathepsin K, which are closely associated with osteoclastogenesis, were significantly downregulated by bavachin in the presence of RANKL. Additionally, bavachin decreased inflammatory molecules, such as nitric oxide, inducible nitric oxide synthase, cyclooxygenase-2, and prostaglandin E2 in RAW264.7 cells treated with RANKL. Bavachin suppressed the RANKLinduced phosphorylation of nuclear factor-κB and subsequently inhibited the translocation of nuclear factor-κB from the cytosol to the nucleus. Taken together, the obtained data suggest that bavachin may prevent the osteoclast-mediated bone destructive disorders.
키워드
Bavachin; Phytoestrogen; Osteoclast; Receptor activator of nuclear factor-κB ligand; Osteoclastogenesis
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