Salvianolic acid B protects against UVB-induced HaCaT cell senescence and skin aging through NRF2 activation and ROS scavenging

Abstract

Background

Prolonged sunlight exposure can cause skin photoaging. The epidermis, the outermost layer of the skin, protects the body from the environment. This study explored the protective effect of salvianolic acid B (Sal-B), a bioactive compound from Salvia miltiorrhiza, against photoaging and examined its specific mechanism.

Methods

In vitro, HaCaT cells were treated with various doses of Sal-B before ultraviolet B (UVB) light exposure. Assessments in HaCaT cells included cellular senescence, apoptotic cell ratio, reactive oxygen species (ROS) levels, mitochondrial function, superoxide dismutase activity, and gene and protein expression. Immunofluorescence labeling, nuclear factor erythroid 2-related factor 2 (NRF2) knockdown, and Western blotting analysis were used. To assess Sal-B's protective effects on skin photoaging in vivo, we employed a nude mouse model and an ex vivo human skin model.

Results

In vitro, Sal-B significantly activated NRF2, scavenged ROS, protected mitochondrial function, and inhibited nuclear factor kappa B and mitogen-activated protein kinase pathways. Ultimately, Sal-B prevented UVB-induced photoaging and keratinocyte apoptosis. In vivo, we confirmed that Sal-B improved skin wrinkles and epidermal thickness in nude mice following UVB irradiation, displaying greater efficacy than tretinoin.

Conclusion

We identified the preventive implications of Sal-B against UVB-induced senescence in skin photoaging and revealed its potential as a regulator of the NRF2 signaling pathway.