A hydrogen-releasing nanozyme may slow osteoarthritis by reducing , inflammation, mitochondrial damage, and cartilage matrix breakdown.
Evidence
This preclinical nanozyme study tested Se-HMPB@AB@COS in osteoarthritis-related chondrocyte mechanisms and in vivo models, reporting reduced •OH, improved , increased collagen II, lower extracellular matrix degradation, and reduced inflammatory factors.
Caveat
The abstract reports mechanistic and in vivo preclinical evidence, not human clinical outcomes or comparative treatment durability.
Simplified
Osteoarthritis (OA), a chronic and degenerative joint disease, has become increasingly prevalent due to the aging population, posing a significant societal burden. However, despite progress, effective therapeutic options for osteoarthritis remain limited. In OA, chronic inflammation mediates a hypoxic microenvironment, leading to increased cellular energy demands. Over time, this causes mitochondrial dysfunction, favoring the accumulation of ROS, thereby perpetuating inflammation. Furthermore, reduced autophagy in aging chondrocytes hinder the clearance of damaged mitochondria, exacerbating . Herein, we have developed a simple and environmentally friendly strategy to fabricate hydrogen-releasing nanozymes (Se-HMPB@AB@COS) that spontaneously release hydrogen gas, effectively treating osteoarthritis through antioxidant, anti-inflammatory, and mitochondrial dysfunction reversal mechanisms. During the process of hydrogen therapy, small hydrogen molecules can readily penetrate mitochondria, specifically reducing the levels of •OH thereby protecting mitochondrial function. Our research further unveils that hydrogen therapy can effectively enhance and delay chondrocyte senescence. In vivo, Se-HMPB@AB@COS encapsulated with chondroitin sulfate significantly promotes the synthesis of collagen II, inhibits the degradation of extracellular matrix, and reduces inflammatory factors. Overall, this study innovatively synthesized a hydrogen-releasing nanozyme, demonstrating its effectiveness in inhibiting oxidative stress, inflammation, promoting mitophagy and extracellular matrix synthesis, thereby reducing cartilage and mitochondrial damage, and delaying OA progression.
Key numbers
59.7%
Osteophyte Size Reduction
Decrease in osteophyte size and maturity after treatment with .
48.7%
BV/TV Value
Bone volume to total volume ratio in the group.
N/A
Collagen II Increase
Enhanced collagen II synthesis observed with treatment.
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