Berberine Inhibits Acne-Related Lipid Secretion and Inflammation by Regulating the hsa-miR-3150a-3p/TP53 Pathway

Acne is a common skin illness that damages both the appearance and mental health of sufferers. The purpose of this study was to investigate the therapeutic value of berberine (BBR) in acne. Firstly, TP53 was mined to be the hub gene through network pharmacology. Then, hsa-miR-3150a-3p was predicted to be the upstream miRNA of TP53 by the ENCORI/starBase database, and their expressions and targeting relationship were verified by RT-qPCR/Western blot and dual-luciferase reporter experiment, respectively. Overexpressing hsa-miR-3150a-3p and TP53 to investigate their roles in lipid secretion and inflammation of biofilm-derived Cutibacterium acnes (Bio-C. acnes)-induced sebocytes. 40 μM of BBR was used to evaluate its effect on sebocyte function. The secretion of fatty acid, triglyceride, IL-6, and IFN-γ was detected by the specific ELISA kit. Hsa-miR-3150a-3p inhibited TP53 expression by targeting its 3'UTR. BBR hindered C. acnes growth and biofilm formation in a concentration-dependent manner. BBR decreased the lipid secretion capacity and inflammatory response in Bio-C. acnes-treated sebocytes, which were synergistically enhanced by TP53 overexpression and were reversed by up-regulation of hsa-miR-3150a-3p. BBR alleviated acne symptoms caused by Bio-C. acnes via the hsa-miR-3150a-3p/TP53 axis.