골격근 미세환경 선택적 상전이를 갖는 활성산소 반응형 주입가능 전도성 하이드로겔 개발 = Skeletal Muscle Microenvironment Selective Sol–Gel Irreversibility of ROS-responsive Injectable and Conductive Hydrogel for Suppressing Muscle Atrophy

다국어 초록 (Multilingual Abstract)

Title: Skeletal Muscle Microenvironment Selective Sol–Gel Irreversibility of ROS-responsive Injectable and Conductive Hydrogel for Suppressing Muscle Atrophy A musculoskeletal disease-associated irreversible phase change [Sol （4°C）-Gel （37°C）-Gel （4°C）] against reversible [Sol （4°C）-Gel （37°C）-Sol （4°C）] phase transition in normal condition forms the basis for an injectable reactive oxygen species （ROS）-scavenging hydrogel （MnO2@PD-HGC） using MnO2-incorporated polymer dots （MnO2@PD） embedded into hexanoyl glycol chitosan （HGC）. The disease-microenvironment-responsive injectable and conductive hydrogel influences the promotion of functional muscle recovery via the cleavage of MnO2 in the presence of ROS inducing an imbalance of hydrophobic interactions to generate the naked-eye detectable irreversible gelation of MnO2@PD-HGC. The cleavage of MnO2 in sarcopenia-microenvironment impacts the resistance of MnO2@PD-HGC （ΔR increases by 184% from 0 to 12 h at 37oC） owing to the formation of Mn2+ alongside the regain of fluorescence via alleviation of FRET. Additionally, analysis with dexamethasone-induced inflammation of C2C12 in a muscle atrophy model highlights the role of sarcopenia- microenvironment sensitive irreversible phase change-based MnO2@PD-HGC hydrogel in scavenging ROS and suppressing sarcopenia via the downregulation of muscle degrading proteins Atrogin-1 and MuRF-1. Finally, in vivo analysis with sarcopenia-induced mice demonstrates the therapeutic capability of MnO2@PD-HGC in influencing skeletal muscle regeneration with an increase in muscle fiber size alongside the real-time wireless response illustrating its ability as a cutting-edge therapeutic and monitoring platform.

목차 (Table of Contents)

• I. Introduction 1
• II. Experimental Section 3
• III. Results and Discussion 10
• IV. Conclusion 64
• V. References 65