Chondroitin sulfate and collagen peptides co-derived from sturgeon cartilage: Characterization and combined effects on IL-1β-induced chondrocyte inflammation in vitro.

Authors

Cheng Ji, Chunyu Niu, Qi Liu, Yan Chen, Qi Zeng, Yin Chen

Published in

International journal of biological macromolecules. Pages 154169. Sep 06, 2026. Epub Sep 06, 2026.

Abstract

Osteoarthritis (OA) is a major joint disorder characterized by cartilage matrix degradation and inflammatory responses. Chondroitin sulfate and collagen peptides are major components of cartilage extracellular matrix and have potential relevance to OA-related inflammation. Sturgeon cartilage, a major processing by-product, is an underutilized source of these bioactive fractions. However, their extraction, characterization, and combined effects on chondrocyte inflammatory responses remain insufficiently studied. In this study, chondroitin sulfate and collagen peptides were separately extracted from sturgeon cartilage. Chondroitin sulfate fraction 1 (CS-1) was obtained by ion-exchange chromatography, whereas collagen peptide fraction 3 (CP-F3) was prepared by enzymatic hydrolysis, ultrafiltration, and gel filtration chromatography. CS-1 was predominantly chondroitin 4-sulfate, with a weight-average molecular weight of approximately 3.0 × 10⁵ Da. CP-F3 was a low-molecular-weight collagen peptide fraction enriched in peptide-related ions below m/z 500. In an IL-1β-induced inflammatory model in SW1353 chondrocyte-like cells, combined treatment with CS-1 and CP-F3 increased proteoglycan and type II collagen retention, reduced NO, iNOS, COX-2, PGE2, and IL-6 levels, and restored the MMP-3/MMP-13/TIMP-1 balance. These effects may be associated with modulation of the TLR4/MyD88/NF-κB signaling pathway. Overall, these findings provide preliminary in vitro evidence that CS-1 and CP-F3, particularly in combination, may attenuate inflammatory and matrix-degrading responses. Further in vivo and mechanistic studies are required to clarify their relevance to cartilage protection.

PMID:
42702320
Bibliographic data and abstract were imported from PubMed on 07 Sep 2026.

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