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<p>Osteoarthritis (OA) is a progressive whole-joint disorder involving cartilage degeneration, oxidative stress, synovial inflammation, and subchondral bone remodeling. Current treatments mainly provide symptomatic relief and rarely restore joint microenvironmental homeostasis. Here, we developed a multifunctional near-infrared (NIR)-responsive CuTA@PDA@PTH nanozyme, termed CPP, for OA therapy. CPP was constructed through copper–tannic acid coordination, polydopamine coating, and PTH 1–34 incorporation, integrating antioxidant catalytic activity, photothermal responsiveness, and peptide-mediated bioactivity. CPP exhibited uniform morphology, good dispersibility, stable photothermal behavior, and broad-spectrum ROS-scavenging activity with SOD-like and CAT-like functions. In vitro, NIR-activated CPP reduced H₂O₂-induced ROS accumulation, lipid peroxidation, mitochondrial dysfunction, and apoptosis in chondrocytes, while promoting proliferation and restoring cartilage matrix homeostasis. CPP-NIR also downregulated inflammatory and catabolic markers, attenuated M1-associated activation, favored an anti-inflammatory M2-like phenotype, and enhanced BMSC migration and osteogenic differentiation under oxidative stress. In a DMM-induced mouse OA model, intra-articular CPP combined with NIR irradiation prolonged joint retention, attenuated cartilage degeneration, reduced osteophyte formation, improved subchondral bone microarchitecture, and alleviated synovial inflammation. These findings support NIR-activated CPP as a multi-axis nanozyme platform for redox, immune, cartilage, and subchondral bone microenvironment regulation in OA.</p>

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Near-infrared-activated CuTA@PDA@PTH nanozymes remodel the osteoarthritic microenvironment for coordinated cartilage protection and subchondral bone repair

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月27日

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  • Zhao Lin,
  • Jiayao Zhang,
  • Mingjuan Zhang,
  • Mukun Xiao,
  • Hanhao Dai,
  • Yibin Su,
  • Haiqi Ding,
  • Dingqiang Chen,
  • Linhai Yang,
  • Jie Xu,
  • Jun Luo,
  • Yunlong Yu

摘要

Osteoarthritis (OA) is a progressive whole-joint disorder involving cartilage degeneration, oxidative stress, synovial inflammation, and subchondral bone remodeling. Current treatments mainly provide symptomatic relief and rarely restore joint microenvironmental homeostasis. Here, we developed a multifunctional near-infrared (NIR)-responsive CuTA@PDA@PTH nanozyme, termed CPP, for OA therapy. CPP was constructed through copper–tannic acid coordination, polydopamine coating, and PTH 1–34 incorporation, integrating antioxidant catalytic activity, photothermal responsiveness, and peptide-mediated bioactivity. CPP exhibited uniform morphology, good dispersibility, stable photothermal behavior, and broad-spectrum ROS-scavenging activity with SOD-like and CAT-like functions. In vitro, NIR-activated CPP reduced H₂O₂-induced ROS accumulation, lipid peroxidation, mitochondrial dysfunction, and apoptosis in chondrocytes, while promoting proliferation and restoring cartilage matrix homeostasis. CPP-NIR also downregulated inflammatory and catabolic markers, attenuated M1-associated activation, favored an anti-inflammatory M2-like phenotype, and enhanced BMSC migration and osteogenic differentiation under oxidative stress. In a DMM-induced mouse OA model, intra-articular CPP combined with NIR irradiation prolonged joint retention, attenuated cartilage degeneration, reduced osteophyte formation, improved subchondral bone microarchitecture, and alleviated synovial inflammation. These findings support NIR-activated CPP as a multi-axis nanozyme platform for redox, immune, cartilage, and subchondral bone microenvironment regulation in OA.