Isoxanthanol has protective and anti-inflammatory effects on subchondral bone deterioration in experimental osteoarthritic rat model

  • Xin li Department of Orthopedics, South of Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Huangcun, Daxing District, Beijing 100053, China
  • Jie Yu Department of Orthopedics, South of Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Huangcun, Daxing District, Beijing 100053, China
  • Yan Zhao Department of Orthopedics, South of Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Huangcun, Daxing District, Beijing 100053, China
  • Yating Bai Department of Emergency, People’s Hospital of Beijing Daxing District, Daxing District, Beijing 102600, China
  • Lixin Fu Department of Orthopedics, South of Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Huangcun, Daxing District, Beijing 100053, China
  • Zilong Ma Department of Orthopedics, South of Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Huangcun, Daxing District, Beijing 100053, China
  • Shuqin Zhang Department of Orthopedics, South of Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Huangcun, Daxing District, Beijing 100053, China
DOI: https://doi.org/10.18388/abp.2020_5634

Abstract

In the present study isoxanthanol was investigated for treatment of monosodium iodoacetate (MIA)-induced osteoarthritis (OA) in vivo. The study demonstrated that isoxanthanol inhibited excessive release of interleukin-6, NO and PGE2 in RAW264.7 cells treated with LPS in dose dependent manner. The effects of isoxanthanol were examined in a rat model of osteoarthritis (OA) and observed to amelio­rate inflammatory damage and protect against OA. Moreover, in vivo data also confirmed inhibition of interleukin-6, NO and PGE2 levels in LPS-induced OA-rats. Deterioration of knee subchondral bone in LPS-induced OA-rats was also prevented effectively by isoxanthanol-treatment. Therefore, isoxanthanol prevents subchondral bone deterioration in OA rats via targeting inflammatory processes.

Published
2022-02-07
Issue
Vol. 69 No. 1 (2022)
Section
Articles

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