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- W2747488488 abstract "Ankylosing spondylitis (AS) is characterized by osteoclastogenesis and inflammatory bone resorption. The present study aimed to investigate the effect of bromodomain and extra-terminal domain (BET) protein inhibitor I-BET151 on AS process. A total of 38 AS Chinese patients were recruited and a further 38 sex- and age-matched healthy participants were selected as control. The Bath AS Function Index and Bath AS Disease Activity Index were assessed in AS patients and levels of erythrocyte sedimentation rate and C-reactive protein were measured in AS and healthy groups. Serum from AS patients was used to induce MG63 osteoblasts and BET inhibitor I-BET151 at concentrations of 50, 100 and 200 ng/ml used for treatment of the cells. A HLA-B27/β2m transgenic AS Lewis rat model was established and treated with 30 mg/kg I-BET151 for 5 weeks. Levels of receptor activator of nuclear factor-κB ligand (RANKL), osteoprotegerin (OPG), matrix metalloproteinase (MMP)3, and MMP9 were measured using ELISA in vivo and additionally detected with western blotting and polymerase chain reaction in vitro. The levels of RANKL, OPG, MMP3 and MMP9 were upregulated in AS serum, AS serum treated MG63 cells and HLA-B27/β2m transgenic AS rats. Conversely, levels of RANKL, OPG, MMP3 and MMP9 were significantly inhibited in cells or animals treated with I-BET151. Overall, the results of the present study demonstrated that BET inhibitor I-BET151 suppresses levels of RANKL, OPG, MMP3 and MMP9 in AS in vivo and in vitro. I-BET151 may exhibit the potential to be used as a therapeutic in the treatment of AS patients." @default.
- W2747488488 created "2017-08-31" @default.
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- W2747488488 date "2017-08-25" @default.
- W2747488488 modified "2023-10-14" @default.
- W2747488488 title "I‑BET151 inhibits expression of RANKL, OPG, MMP3 and MMP9 in ankylosing spondylitis in�vivo and in�vitro" @default.
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- W2747488488 doi "https://doi.org/10.3892/etm.2017.5032" @default.
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