Bavachin counteracts receptor activator of nuclear factor-κB-induced osteoclastogenesis though the suppression of nuclear factor-κB signaling pathway in RAW264.7 cells
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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.
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.
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