Emodin combined with ALA-PDT for the treatment of acne by targeting the SerRS-ACC1 pathway to inhibit lipid synthesis

Increased sebum secretion and infection with P.acnes are important causes of acne vulgaris. The aim of this study was to investigate the efficacy of emodin combined with ALA-PDT in the treatment of acne vulgaris and the mechanism of sebaceous secretion regulation. The Hacat cell model and the acne-like mouse ear model were treated with emodin, ALA-PDT, and emodin combined with ALA-PDT, respectively. Skin inflammation, SerRS and ACC1 expression were measured using qRT-PCR and Western blot. Emodin combined with ALA-PDT can significantly inhibit the proliferation and promote its apoptosis and ROS production in vitro. It can significantly reduce the secretion of pro-inflammatory factors. Mechanistically, emodin combined with ALA-PDT could promote the expression of SerRS, and SerRS can transcriptionally suppress its expression by binding to the promoter of ACC1. Our study provides a novel insight that emodin combined with ALA-PDT can inhibit lipid synthesis via the SerRS-ACC1 axis and thus treat acne.