Q‐switched 1064 nm Nd: YAG laser restores skin photoageing by activating autophagy by TGFβ1 and ITGB1

Abstract

AbstractExcessive ultraviolet B ray (UVB) exposure to sunlight results in skin photoageing. Our previous research showed that a Q‐switched 1064 nm Nd: YAG laser can alleviate skin barrier damage through miR‐24‐3p. However, the role of autophagy in the laser treatment of skin photoageing is still unclear. This study aims to investigate whether autophagy is involved in the mechanism of Q‐switched 1064 nm Nd: YAG in the treatment of skin ageing. In vitro, primary human dermal fibroblast (HDF) cells were irradiated with different doses of UVB to establish a cell model of skin photoageing. In vivo, SKH‐1 hairless mice were irradiated with UVB to establish a skin photoageing mouse model and irradiated with laser. The oxidative stress and autophagy levels were detected by western blot, immunofluorescence and flow cytometer. String was used to predict the interaction protein of TGF‐β1, and CO‐IP and GST‐pull down were used to detect the binding relationship between TGFβ1 and ITGB1. In vitro, UVB irradiation reduced HDF cell viability, arrested cell cycle, induced cell senescence and oxidative stress compared with the control group. Laser treatment reversed cell viability, senescence and oxidative stress induced by UVB irradiation and activated autophagy. Autophagy agonists or inhibitors can enhance or attenuate the changes induced by laser treatment, respectively. In vivo, UVB irradiation caused hyperkeratosis, dermis destruction, collagen fibres reduction, increased cellular senescence and activation of oxidative stress in hairless mice. Laser treatment thinned the stratum corneum of skin tissue, increased collagen synthesis and autophagy in the dermis, and decreased the level of oxidative stress. Autophagy agonist rapamycin and autophagy inhibitor 3‐methyladenine (3‐MA) can enhance or attenuate the effects of laser treatment on the skin, respectively. Also, we identified a direct interaction between TGFB1 and ITGB1 and participated in laser irradiation‐activated autophagy, thereby inhibiting UVB‐mediated oxidative stress further reducing skin ageing. Q‐switched 1064 nm Nd: YAG laser treatment inhibited UVB‐induced oxidative stress and restored skin photoageing by activating autophagy, and TGFβ1 and ITGB1 directly incorporated and participated in this process.