Solar dermatitis, a form of acute radiation burn that affects the skin, results from overexposure to ultraviolet B (UVB) radiation in strong sunlight. Cell damage caused by the accumulation of reactive oxygen species (ROS) produced by UVB radiation plays an important role in UVB-induced inflammation in the skin. Here, for efficiently scavenging excess ROS, modulating the microenvironment, and alleviating solar dermatitis, a π-conjugated network polyphthalocyanine supporting a highly surface-exposed Ru active site-based artificial antioxidase (HSE-PPcRu) is designed and fabricated with excellent ROS-scavenging, antioxidant, and anti-inflammatory capabilities. In photodamaged human keratinocyte cells, HSE-PPcRu could modulate mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B signaling pathways, prevent DNA damage, suppress apoptosis, inhibit pro-inflammatory cytokine secretion, and alleviate cell damage. In vivo animal experiments reveal the higher antioxidant and anti-inflammatory efficacies of HSE-PPcRu by reversing the activation of p38 and c-Jun N-terminal kinase, inhibiting expression of cyclooxygenase-2, interleukin-6, interleukin-8, and tumor necrosis factor-α. This work not only provides an idea for alleviating solar dermatitis via catalytically scavenging ROS and modulating the microenvironment but also offers a strategy to design an intelligent conjugated network-based artificial antioxidase with a highly surface-exposed active site.
Keyphrases
- oxidative stress
- dna damage
- reactive oxygen species
- signaling pathway
- nuclear factor
- anti inflammatory
- induced apoptosis
- diabetic rats
- cell death
- single cell
- cell cycle arrest
- toll like receptor
- stem cells
- photodynamic therapy
- dna repair
- atopic dermatitis
- cell therapy
- wound healing
- endothelial cells
- poor prognosis
- epithelial mesenchymal transition
- drug induced
- liver failure
- soft tissue
- rheumatoid arthritis
- immune response
- genome wide
- radiation induced
- high glucose
- respiratory failure
- hepatitis b virus
- inflammatory response
- cell proliferation
- dna methylation
- gene expression
- nitric oxide
- quantum dots