Antarctic Krill Oil Ameliorates Monosodium Iodoacetate-Induced Irregularities in Articular Cartilage and Inflammatory Response in the Rat Models of Osteoarthritis

• Published in: Nutrients 2020-11, Vol.12 (11), p.3550
• Main Authors: Lee, Minhee, Kim, Dakyung, Park, Soo-Jeung, Yun, Jeong Moon, Oh, Dong Hwan, Lee, Jeongmin
• Format: Article
• Language: English
• Subjects: Animal models; Animals; Antarctic krill oil; Antarctic Regions; Arthritis; Biomedical materials; Bone density; Cartilage; Cartilage (articular); Cartilage diseases; Cartilage, Articular - drug effects; Cartilage, Articular - pathology; Chemical compounds; Collagen; Computed tomography; Cytokines; Cytokines - blood; Degeneration; Diet; Dietary supplements; Disease Models, Animal; Euphausiacea - chemistry; Functional foods & nutraceuticals; Gene expression; IL-1β; Inflammation; Inflammatory response; Interleukin 6; Iodoacetates - adverse effects; Iodoacetic Acid - adverse effects; Irregularities; Krill; Male; monoiodoacetate; Oils - pharmacology; Osteoarthritis; Osteoarthritis - drug therapy; Osteoarthritis - pathology; Pain; Pharmacology; Polar environments; Prostaglandin E2; Rats; Rats, Sprague-Dawley; RNA, Messenger - metabolism; Rodents; Statistical analysis; Tumor necrosis factor-α; X-Ray Microtomography
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu12113550

The aim of this study was to examine the effects of Antarctic krill oil (FJH-KO) in a rat model of monosodium iodoacetate (MIA) induced osteoarthritis. The effect of FJH-KO on the development and severity of MIA-induced osteoarthritis was assessed using hematoxylin and eosin (H&E) staining and micro-CT. The expression of PGE , pro-inflammatory cytokines (IL-1β, TNF-α), and arthritics related genes in osteoarthritic rats in response to FJH-KO supplementation was investigated using real time PCR. FJH-KO supplementation in the arthritic rat model reduced tissue damage, cartilage degeneration, and reduced the MIA-induced irregularities in articular cartilage surface. Serum PGE , IL-1β, IL-6, and TNF-α levels were higher in MIA treated animals, but these levels decreased upon FJH-KO supplementation. When FJH-KO was provided at a dose of 150 mg/kg b.w to MIA-treated animals, it significantly increased the mRNA expression of anabolic factors. The mRNA expression of catabolic factors was significantly decreased MIA-treated animals that were provided FJH-KO at a dose of 100 and 150 mg/kg b.w. Moreover, the mRNA expression of inflammatory mediators was significantly decreased MIA-treated animals supplemented with FJH-KO. These results suggest supplementation with FJH-KO ameliorates the irregularities in articular cartilage surface and improves the inflammatory response in the osteoarthritis. Thus, FJH-KO could serve as a potential therapeutic agent for osteoarthritis treatment.