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

Background: Acne is a common skin illness that damages both the appearance and mental health of sufferers.

Objective: The purpose of this study was to investigate the therapeutic value of berberine (BBR) in acne.

Methods: 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.

Results: 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.

Conclusion: BBR alleviated acne symptoms caused by Bio-C. acnes via the hsa-miR-3150a-3p/TP53 axis.

Cutibacterium acnes; berberine; inflammation; lipid secretion; sebocytes.