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This Research Provides New Insights for Alleviating UVB-Induced Photodermatitis

YangChen Sun, May 12 2024 10:48 AM EST

Recently, a collaborative team of researchers from the Ultrasonic Medicine Research Laboratory at West China Hospital of Sichuan University led by Dr. Malang published a research article in "Nanotechnology." The study introduced a novel artificial antioxidant enzyme with a highly exposed active center and a conjugated network structure, named HSE-PPcRu. This enzyme demonstrated the ability to eliminate reactive oxygen species (ROS) activity, regulate ROS-related pathways within cells to reduce UVB-induced cellular damage, and alleviate skin inflammation caused by UVB exposure. The research provides a new strategy for designing an artificial antioxidant enzyme with an active site highly exposed based on a conjugated network.

Excessive exposure of the skin to ultraviolet radiation can lead to inflammation, aging, and skin damage such as tumors. The primary cause of UV-induced photodermatitis is the accumulation of ROS in tissues due to UV radiation. Therefore, the key to alleviating UV-induced photodermatitis is to reduce the excessive accumulation of ROS in tissues and regulate the inflammatory factors in the microenvironment.

HSE-PPcRu exhibits excellent catalase (CAT) and superoxide dismutase (SOD) activities, capable of scavenging hydrogen peroxide (H2O2) and superoxide anions (·O2-). Enzyme catalytic activity per unit Ru wt% was calculated using XPS, showing that HSE-PPcRu has superior CAT and SOD activities compared to the control sample, along with good stability. Furthermore, a comprehensive comparison with recently reported ROS-scavenging nanoenzymes such as Co3O4 nanorods, Mn3O4, Au24Cu1, and single-atom nanoenzyme Rh-N4 revealed that HSE-PPcRu exhibited superior CAT-like activity.

By regulating ROS-related pathways and reducing MAPK phosphorylation to decrease apoptosis in HaCaT cells, as well as modulating the NF-κB inflammatory pathway to reduce the secretion of inflammatory factors, HSE-PPcRu effectively alleviates UVB-induced inflammation.

Animal experiments conducted on Balb/c mice also demonstrated that the use of HSE-PPcRu could alleviate UVB-induced photodermatitis in mice by reducing ROS accumulation, inflammatory cell infiltration, epidermal thickness, keratinocyte proportion, and DNA double-strand breaks.

The study highlights that HSE-PPcRu serves as an effective artificial antioxidant enzyme for the broad-spectrum elimination of ROS. The artificial antioxidant enzyme HSE-PPcRu with a conjugated network structure exhibits advantages such as a highly exposed active center, high dispersibility, and high chemical stability. Due to these structural features, HSE-PPcRu shows a stable elimination rate of H2O2 and ·O2-, surpassing most reported artificial antioxidant enzymes in ROS scavenging. Both in vitro and in vivo experiments confirm that HSE-PPcRu reduces ROS-related damage, thereby alleviating UVB-induced photodermatitis. This research provides a promising avenue for designing efficient artificial antioxidant enzymes to alleviate UVB-induced photodermatitis and may serve as an effective clinical strategy.

For more information on the related paper, please visit: https://doi.org/10.1021/acsnano.3c10552