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  Indian J Med Microbiol
 

Figure 6: Alpha-mangostin impaired osteoclastogenesis by inhibiting the extracellular signal-regulated kinase and c-Jun N-terminal kinase signaling pathways and the inhibitory effects were rescued by anisomycin. (a) Cells were pre-treated with or without 0.8 μM alpha-mangostin for 4 h, followed by administrating receptor activator of nuclear factor-κB ligand for 0, 5 or 15 min. The phosphorylated levels of extracellular signal-regulated kinase, p38, c-Jun N-terminal kinase and total nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha were assessed. (b) Cells were treated with/without anisomycin in the presence of alpha-mangostin for 4 days, then stained with tartrate-resistant acid phosphatase solution. (c) Cells were pre-treated with alpha-mangostin for 4 h and then stimulated by receptor activator of nuclear factor-κB ligand with Anisomycin/dimethyl sulfoxide for 5 min. The phosphorylated expression of c-Jun N-terminal kinase was evaluated

Figure 6: Alpha-mangostin impaired osteoclastogenesis by inhibiting the extracellular signal-regulated kinase and c-Jun N-terminal kinase signaling pathways and the inhibitory effects were rescued by anisomycin. (a) Cells were pre-treated with or without 0.8 μM alpha-mangostin for 4 h, followed by administrating receptor activator of nuclear factor-κB ligand for 0, 5 or 15 min. The phosphorylated levels of extracellular signal-regulated kinase, p38, c-Jun N-terminal kinase and total nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha were assessed. (b) Cells were treated with/without anisomycin in the presence of alpha-mangostin for 4 days, then stained with tartrate-resistant acid phosphatase solution. (c) Cells were pre-treated with alpha-mangostin for 4 h and then stimulated by receptor activator of nuclear factor-κB ligand with Anisomycin/dimethyl sulfoxide for 5 min. The phosphorylated expression of c-Jun N-terminal kinase was evaluated