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Walker and Jean Christopher Chamcheu  \nReceived: 1 December 2025  \nRevised: 27 December 2025  \nAccepted: 31 December 2025  \nPublished: 5 January 2026  \nCopyright: © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.  \n1 College of Pharmacy, Chungbuk National University, 194-21 Osongsaengmyoung 1-ro, Osong-eup, Heungduk-gu, Cheongju 29160, Chungbuk, Republic of Korea; [yumin0413@chungbuk.ac.kr](yumin0413@chungbuk.ac.kr) (M.Y.);  \n[lovel5508@chungbuk.ac.kr](lovel5508@chungbuk.ac.kr) (S.E.J.); [yb@chungbuk.ac.kr](yb@chungbuk.ac.kr) (Y.B.S.); [yejinee13@chungbuk.ac.kr](yejinee13@chungbuk.ac.kr) (Y.J.K.);  \n[seoys@chungbuk.ac.kr](seoys@chungbuk.ac.kr) (Y.S.); [shan@chungbuk.ac.kr](shan@chungbuk.ac.kr) (S.B.H.)  \n2 R&D Center, Naturetech Inc., 450-86 Maebong-ro, Byeongcheon-myeon, Dongnam-gu, Cheonan 31257, Chungnam, Republic of Korea; [hjmari@naturetech.co.kr](hjmari@naturetech.co.kr) (H.J.K.);  \n[sgildo@naturetech.co.kr](sgildo@naturetech.co.kr) (S.G.D.)  \n3 Wallace H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, 1760 Haygood Drive NE, Atlanta, GA 30306, USA; [hjo@emory.edu](hjo@emory.edu)  \n* Correspondence: [sondj1@chungbuk.ac.kr](sondj1@chungbuk.ac.kr); Tel.: +82-43-261-2822 † These authors contributed equally to this work.  \nAbstract  \nBackground/Objectives: Osteoarthritis (OA) is a pervasive chronic joint disease characterized by the triad of persistent articular cartilage degeneration, debilitating synovial inflammation, and sustained chronic pain. Although salmon nasal cartilage proteoglycan (SPG) is recognized for supporting joint health, the precise molecular mechanism underlying its effects during OA progression remains to be fully elucidated. This study evaluated the therapeutic efficacy of SPG using a monosodium iodoacetate (MIA)-induced mouse model. Methods: A total of 180 male C57BL/6J mice (six-week-old) were utilized, organized into three independent cohorts to analyze distinct analytical endpoints: (1) pain assessment, histology, and immunohistochemistry; (2) mRNA expression analysis for early-stage OA (Day 3); and (3) mRNA expression analysis for the late-stage OA (Day 28) . All subjects received daily oral treatment via gavage, commencing 5 days prior to OA induction and continuing until the designated experimental termination points (either Day 3 or Day 28) . Each cohort comprised five experimental groups (n = 10–12 per group): a saline-injected Sham group, an MIA-induced Control group, a positive comparator receiving celecoxib (CLX, 20 mg/kg/day), and two groups administered SPG at a dose of 50 or 100 mg/kg/day. Results: Our findings demonstrated that SPG, particularly at the 100 mg/kg dose, significantly mitigated joint pain symptoms, performing comparably to CLX. Histopathological assessments confirmed that SPG effectively preserved the structural integrity of the cartilage matrix and substantially reduced pathological damage, as evidenced by lower Mankin scores. Mechanistically, SPG treatment led to a marked downregulation of degradative enzymes, including matrix metalloproteinase-3 (MMP-3) and a disintegrin and metalloproteinase with thrombospondin motifs 4 (ADAMTS-4), while concurrently normalizing the levels of tissue inhibitors of metalloproteinases (TIMPs) . Furthermore, SPG prevented the aberrant, over-compensatory expression of anabolic markers such as SRY-box transcription factor 9 (SOX-9), type II collagen alpha 1 chain (COL2A","cbCaiulqPs4Z2Zqo","https://ap.wps.com/l/cbCaiulqPs4Z2Zqo","pdf",4752714,"English","# Abstract\n## Background/Objectives\n## Methods\n## Results\n## Conclusions\n# Introduction","[{\"question\":\"What disease model was used to evaluate SPG's effects on osteoarthritis?\",\"answer\":\"The study used a monosodium iodoacetate (MIA)-induced mouse model of osteoarthritis, with treatment given orally via gavage before and through the designated endpoints.\"},{\"question\":\"How did SPG affect joint pain and cartilage damage in the MIA model?\",\"answer\":\"SPG, especially at 100 mg/kg/day, significantly mitigated joint pain and preserved cartilage matrix structure, with reduced pathological damage reflected by lower Mankin scores.\"},{\"question\":\"Which molecular pathways or markers were changed by SPG treatment?\",\"answer\":\"SPG downregulated cartilage-degradative enzymes such as MMP-3 and ADAMTS-4 while normalizing TIMP levels, and it reduced abnormal late-stage increases in anabolic markers like SOX-9, COL2A1, and ACAN.\"}]","Salmon Nasal Cartilage Proteoglycan Ameliorate Joint Pain and Cartilage Degradation by Regulating Catabolic and Anabolic Homeostasis in MIA-Induced Osteoarthritis | PDF",1790773036]