Owing to the increasing popularity of chondroitin sulfate (CS) for joint pain treatment, the CS-production industry has been producing an increasing amount of waste, which includes type II collagen, non-collagenous proteins, and residual CS. To effectively utilize these resources, we intended to develop new products from the by-product of skate chondroitin sulfate production (BP-sCS). In this study, we examined the antioxidant and fibroblast-activating properties of BP-sCS, intending to apply it for a wound-healing promoter. BP-sCS exhibited ABTS and DPPH radical scavenging activities, protected L929 fibroblasts from H₂O₂- or AAPH-induced oxidative stress, and scavenged intracellular reactive oxygen species. Moreover, BP-sCS promoted L929 fibroblast proliferation/metabolism and stimulated collagen deposition into the extracellular matrix. In addition, BP-sCS counteracted AAPH-induced oxidative stress damage that inhibited fibroblast migration. These effect were attributed to the cooperation among the molecules of BP-sCS, namely, type II collagen peptides, non-collagenous peptides, and CS polysaccharides. Our findings indicate that BP-sCS has the potential as a novel wound-healing promoter. This study is the first step toward the realization of a sustainable CS-production industry by waste utilization in healthcare products.

由于硫酸软骨素 (CS) 在治疗关节疼痛方面越来越受欢迎，因此 CS 生产行业产生了越来越多的废物，其中包括 II 型胶原蛋白、非胶原蛋白和残留的 CS。为了有效利用这些资源，我们打算从冰鞋硫酸软骨素生产 (BP-sCS) 的副产品中开发新产品。在这项研究中，我们检查了 BP-sCS 的抗氧化和成纤维细胞激活特性，打算将其应用于伤口愈合促进剂。BP-sCS 表现出 ABTS 和 DPPH 自由基清除活性，保护 L929 成纤维细胞免受 H ₂ O ₂- 或 AAPH 诱导的氧化应激，以及清除细胞内活性氧。此外，BP-sCS 促进 L929 成纤维细胞增殖/代谢并刺激胶原沉积到细胞外基质中。此外，BP-sCS 抵消了抑制成纤维细胞迁移的 AAPH 诱导的氧化应激损伤。这些作用归因于BP-sCS分子之间的合作，即II型胶原肽、非胶原肽和CS多糖。我们的研究结果表明 BP-sCS 具有作为新型伤口愈合促进剂的潜力。这项研究是通过医疗产品中的废物利用实现可持续 CS 生产行业的第一步。