Carbon Dot Nanozyme Ameliorating Ischemia-Reperfusion-Induced Muscle Injury by Antioxidation and Downregulating iNOS/COX-2 Pathway.
Wenbin FanQing-Ying LuoXun LuQing XieQunzeng DanzengYiqian ZhangSong JinWen-Xiang ChengCui LiuPublished in: ACS omega (2024)
Skeletal muscle ischemia-reperfusion (IR) injury is a prevalent type of muscle injury caused by events, such as trauma, arterial embolism, and primary thrombosis. The development of an IR injury is associated with oxidative stress and an excessive inflammatory response. Nanozymes, which have exceptional free radical scavenging activities, have gained significant attention for treating oxidative stress. This study demonstrates that carbon dot (C-dot) nanozymes possess superoxide dismutase (SOD)-like activity and can act as free radical scavengers. The carbon dot nanozymes are presented to mitigate inflammation by downregulating the iNOS/COX-2 pathway and scavenging reactive oxygen-nitrogen species to reduce oxidative stress, thereby suppressing inflammation. In the IR injury of skeletal muscle mice, we demonstrate that C-dots can effectively reduce inflammatory cytokines and tissue edema in skeletal muscle following IR injury in the limb. These findings suggest that C-dots have potential as a therapeutic approach for IR injury of skeletal muscle with negligible systemic toxicity. This offers a promising strategy for clinical intervention.
Keyphrases
- skeletal muscle
- oxidative stress
- diabetic rats
- insulin resistance
- inflammatory response
- dna damage
- randomized controlled trial
- ischemia reperfusion injury
- type diabetes
- induced apoptosis
- working memory
- pulmonary embolism
- physical activity
- high fat diet induced
- high resolution
- metabolic syndrome
- mass spectrometry
- heat shock
- heat stress
- drug induced