Sung-Min Moon1, Seul Ah Lee2, Seul Hee Han3, Bo-Ram Park4, Mi Suk Choi4, Jae-Sung Kim5, Su-Gwan Kim5, Heung-Joong Kim5, Hong Sung Chun6, Do Kyung Kim5, Chun Sung Kim7. 1. Oral Biology Research Institute, College of Dentistry, Chosun University, 375 Seosuk-dong, Dong-gu, Gwangju, 501-759, Republic of Korea; CStech Research Institute, 38 Chumdanventuresoro, Gwangju 61007, Republic of Korea. 2. Department of Oral Biochemistry, College of Dentistry, Chosun University, 375 Seosuk-dong, Dong-gu, Gwangju, 501-759, Republic of Korea. 3. CStech Research Institute, 38 Chumdanventuresoro, Gwangju 61007, Republic of Korea. 4. Department of Dental Hygiene, Chodang University, Muan-ro, Muan-eup, Muan 534-701, Republic of Korea. 5. Oral Biology Research Institute, College of Dentistry, Chosun University, 375 Seosuk-dong, Dong-gu, Gwangju, 501-759, Republic of Korea. 6. Department of Biomedical Science, Chosun University, 375 Seosuk-dong, Dong-gu, Gwangju, 501-759, Republic of Korea. 7. Oral Biology Research Institute, College of Dentistry, Chosun University, 375 Seosuk-dong, Dong-gu, Gwangju, 501-759, Republic of Korea; Department of Oral Biochemistry, College of Dentistry, Chosun University, 375 Seosuk-dong, Dong-gu, Gwangju, 501-759, Republic of Korea. Electronic address: cskim2@chosun.ac.kr.
Abstract
BACKGROUND: Codium fragile (Suringar) Hariot has been used as a potential remedy in traditional medicine because of its anti-inflammatory and anti-oxidant effects. Osteoarthritis is a chronic progressive joint disease, characterized by complex mechanisms related to inflammation and degeneration of articular cartilage. In this study, we aimed to evaluate the cartilage protective effect of an aqueous extract of Codium fragile (AECF) using rat primary chondrocytes and the osteoarthritis animal model induced by destabilization of the medial meniscus (DMM). METHODS: In vitro, rat primary cultured chondrocytes were pre-treated with AECF (0.5, 1, and 2mg/mL) for 1h and then incubated with interleukin-1β (10ng/mL) for 24h. Nitrite production was detected by the Griess reagent. Alteration of the protein levels of iNOS, MMP-13, ADAMTS-4, ADAMTS-5, mitogen-activated protein kinases (MAPKs), and nuclear factor-κB (NF-κB) was detected by western blotting. In vivo, osteoarthritis was induced by DMM of Sprague Dawley (SD) rats. The rats subjected to destabilization of the medial meniscus (DMM) surgery were orally administered with AECF (50, 100, and 200mg/kg bodyweight) or distilled water for 8w. The severity of cartilage lesions was evaluated by safranin O staining and the Osteoarthritis Research Society International (OARSI) score. RESULTS: These results demonstrated that AECF significantly inhibited nitrite production and inhibited the levels of iNOS, MMP-13, ADAMTS-4, and ADAMTS-5 in interleukin-1β-induced rat primary cultured chondrocytes. Moreover, AECF suppressed interleukin-1β-induced NF-κB activation in the nucleus and phosphorylation of ERK1/2 and JNK in the cytosol. In vivo, the cartilage lesions in AECF-treated osteoarthritis rats exhibited less proteoglycan loss and lower OARSI scores. CONCLUSIONS: These results suggested that AECF is a potential therapeutic agent for the alleviation of osteoarthritis progression.
BACKGROUND:Codium fragile (Suringar) Hariot has been used as a potential remedy in traditional medicine because of its anti-inflammatory and anti-oxidant effects. Osteoarthritis is a chronic progressive joint disease, characterized by complex mechanisms related to inflammation and degeneration of articular cartilage. In this study, we aimed to evaluate the cartilage protective effect of an aqueous extract of Codium fragile (AECF) using rat primary chondrocytes and the osteoarthritis animal model induced by destabilization of the medial meniscus (DMM). METHODS: In vitro, rat primary cultured chondrocytes were pre-treated with AECF (0.5, 1, and 2mg/mL) for 1h and then incubated with interleukin-1β (10ng/mL) for 24h. Nitrite production was detected by the Griess reagent. Alteration of the protein levels of iNOS, MMP-13, ADAMTS-4, ADAMTS-5, mitogen-activated protein kinases (MAPKs), and nuclear factor-κB (NF-κB) was detected by western blotting. In vivo, osteoarthritis was induced by DMM of Sprague Dawley (SD) rats. The rats subjected to destabilization of the medial meniscus (DMM) surgery were orally administered with AECF (50, 100, and 200mg/kg bodyweight) or distilled water for 8w. The severity of cartilage lesions was evaluated by safranin O staining and the Osteoarthritis Research Society International (OARSI) score. RESULTS: These results demonstrated that AECF significantly inhibited nitrite production and inhibited the levels of iNOS, MMP-13, ADAMTS-4, and ADAMTS-5 in interleukin-1β-induced rat primary cultured chondrocytes. Moreover, AECF suppressed interleukin-1β-induced NF-κB activation in the nucleus and phosphorylation of ERK1/2 and JNK in the cytosol. In vivo, the cartilage lesions in AECF-treated osteoarthritisrats exhibited less proteoglycan loss and lower OARSI scores. CONCLUSIONS: These results suggested that AECF is a potential therapeutic agent for the alleviation of osteoarthritis progression.
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