Effects of salmon DNA fraction in vitro and in a monosodium iodoacetate-induced osteoarthritis rat model.
10.4196/kjpp.2018.22.2.163
- Author:
Ho Jong RA
1
;
Mi Young OH
;
Hee Ju KIM
;
Seung Yong LEE
;
Dae Woon EOM
;
Suk Kyu LEE
;
Su Nam KIM
;
Kyu Sung CHUNG
;
Hyuk Jai JANG
Author Information
1. Department of Orthopedic Surgery, Gangneung Asan Hospital, Ulsan University College of Medicine, Gangneung 25440, Korea.
- Publication Type:Original Article
- Keywords:
Chondrocyte;
Cytokine;
Inflammation;
Osteoarthritis;
Polydeoxyribonucleotide;
PRF001
- MeSH:
Animals;
Arthritis;
Cartilage, Articular;
Cell Survival;
Chondrocytes;
Cytokines;
Dinoprostone;
DNA*;
In Vitro Techniques*;
Inflammation;
Injections, Intra-Articular;
Knee Joint;
Matrix Metalloproteinases;
Models, Animal*;
Osteoarthritis*;
Polymers;
Rats*;
Salmon*;
Testis
- From:The Korean Journal of Physiology and Pharmacology
2018;22(2):163-172
- CountryRepublic of Korea
- Language:English
-
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 H₂O₂ 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-1β, TNF-α, COX-2, iNOS, and PGE2, were significantly suppressed by PRF001 treatment. In vivo, the inflammatory mediators and cytokines, IL-1β, p-Erk1/2, NF-κB, TNF-α, 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-1β, TNF-α, and subsequent signals, such as p-Erk1/2, NF-κB, COX-2, PGE2, and MMPs.
