Abstract
Autophagy is a protective mechanism in normal cartilage. The present study aimed to investigate the synergistic therapeutic effect of promotion of chondrocyte autophagy via exposure to cordycepin encapsulated by chitosan microspheres (CM-cordycepin) and photo-crosslinked hyaluronic acid methacrylate (HAMA) hydrogel, with the goal of evaluating CM-cordycepin as a treatment for patients with osteoarthritis. First, we developed and evaluated the characteristics of HAMA hydrogels and chitosan microspheres. Next, we measured the effect of cordycepin on cartilage matrix degradation induced by IL1-β in chondrocytes and an ex vivo model. Cordycepin protects cartilage from degradation partly by activation of autophagy. Moreover, we surgically induced osteoarthritis in mice, which were injected intra-articularly with CM-cordycepin and HAMA. The combination of CM-cordycepin and HAMA hydrogel retarded the progression of surgically induced OA. Cordycepin ameliorated cartilage matrix degradation at least partially by inducing autophagy in vivo. Our results demonstrate that the combination of cordycepin encapsulated by CMs and photo-crosslinked HAMA hydrogel could be a promising strategy for treating patients with osteoarthritis.
Highlights
Osteoarthritis (OA) is becoming more problematic as the population ages
The present study aimed to investigate the synergistic therapeutic effect of promotion of chondrocyte autophagy via exposure to cordycepin encapsulated by chitosan microspheres (CM-cordycepin) and photo-crosslinked hyaluronic acid methacrylate (HAMA) hydrogel, with the goal of evaluating Chitosan microspheres (CMs)-cordycepin as a treatment for patients with osteoarthritis
Our results demonstrate that the combination of cordycepin encapsulated by CMs and photo-crosslinked HAMA hydrogel could be a promising strategy for treating patients with osteoarthritis
Summary
Osteoarthritis (OA) is becoming more problematic as the population ages. Patients with OA experience variable degrees of inflammation and degeneration of the articular cartilage, resulting in exposure of the underlying bone, pain, and disability [1, 2]. Structure-modifying medications and nutraceuticals may be effective therapeutic agents for OA and merit further investigation [3]. Autophagy is the physiological cellular process through which intracellular components undergo lysosomemediated self-digestion and recycling, and this process is essential for survival, differentiation, development, and homeostasis [4, 5]. Autophagy is a protective mechanism in normal cartilage [6]. Reduced expression of autophagy regulators was observed in pathological cartilage in humans and mice [7]. Activation of autophagy by rapamycin treatment reduced the severity of OA in experimental models [8]. Autophagy activation may be a novel therapeutic target for OA treatments. LC3 is recruited to the autophagosomal membrane [10]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
