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Effects of salmon DNA fraction in vitro and in a monosodium iodoacetate-induced osteoarthritis rat model

  • Ra, Ho Jong (Department of Orthopedic Surgery, Gangneung Asan Hospital, Ulsan University College of Medicine) ;
  • Oh, Mi Young (Medical Research Institute, Gangneung Asan Hospital) ;
  • Kim, Hee Ju (Medical Research Institute, Gangneung Asan Hospital) ;
  • Lee, Seung Yong (Medical Research Institute, Gangneung Asan Hospital) ;
  • Eom, Dae Woon (Department of Pathology, Gangneung Asan Hospital, Ulsan University College of Medicine) ;
  • Lee, Suk Kyu (Department of Orthopedic Surgery, Gangneung Asan Hospital, Ulsan University College of Medicine) ;
  • Kim, Su-Nam (Natural Products Research Institute, Korea Institute of Science and Technology) ;
  • Chung, Kyu Sung (Department of Orthopedic Surgery, Hanil General Hospital) ;
  • Jang, Hyuk Jai (Department of Surgery, Gangneung Asan Hospital, Ulsan University College of Medicine)
  • Received : 2017.09.08
  • Accepted : 2018.01.27
  • Published : 2018.03.01

Abstract

PRF001 is a fragmented DNA polymer extracted from the testes of salmon. The purpose of this study was to assess the anti-inflammatory effect of PRF001 in vitro as well as the protective effect of PRF001 intake against arthritis in a rat model. In vitro, cell survival and inflammatory markers after $H_2O_2$ treatment to induce cell damage were investigated in CHON-001 cells treated with different concentrations of PRF001. In vivo, osteoarthritis was induced by intra-articular injection of monosodium iodoacetate (MIA) into the knee joints of rats. After consumption of PRF001 (10, 50, or 100 mg/kg) for 4 weeks, inflammatory mediators and cytokines in articular cartilage were investigated. In vitro, the levels of inflammatory markers, $IL-1{\beta}$, $TNF-{\alpha}$, COX-2, iNOS, and PGE2, were significantly suppressed by PRF001 treatment. In vivo, the inflammatory mediators and cytokines, $IL-1{\beta}$, p-Erk1/2, $NF-{\kappa}B$, $TNF-{\alpha}$, COX-2, and PGE2, as well as MMP3 and MMP7, which have catabolic activity in chondrocytes, were decreased in the MIA-induced osteoarthritic rats following intake of PRF001. Histological analysis revealed that PRF001 had a protective effect on the articular cartilage. Altogether, these results demonstrated that the anti-inflammatory property of PRF001 contributes to its protective effects in osteoarthritis through deregulating $IL-1{\beta}$, $TNF-{\alpha}$, and subsequent signals, such as p-Erk1/2, $NF-{\kappa}B$, COX-2, PGE2, and MMPs.

Keywords

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