Protective Effect of Berberine on Atopic Dermatitis by Regulating the lncRNA TTC39A-AS1/hsa-miR-3936/RNASE3 axis

Abstract

Colonization of Staphylococcus aureus (S. aureus) is a crucial factor aggravating atopic dermatitis (AD). Berberine (BBR) is the main effective component of Coptis chinensis against bacteria. To explore the potential mechanism by which BBR inhibits the progression of AD caused by S. aureus. S. aureus was cultured with a BBR-added medium to verify the bacteriostatic effect of BBR. Effects of BBR on the expressions of TTC39A-AS1, hsa-miR-3936, and RNASE3 were detected by qPCR, and the dual luciferase assay and overexpression assay were used to demonstrate the regulation among them. The roles of them in S. aureus-induced injury of human primary epidermal keratinocytes (HEKs) were evaluated by their exogenous expressions. The growth, inflammation, and tight junction were evaluated by CCK-8 assay, detection of inflammatory factors, and measurement of transepithelial electrical resistance (TEER) value, to evaluate the impairment of HEKs. BBR significantly inhibited the reproduction of S. aureus and improved the damage to HEKs function caused by it. The stimulation of S. aureus significantly inhibited the growth and tight junction function of HEKs and induced the inflammatory response. These changes were exacerbated by overexpression of TTC39A-AS1 or RNASE3, and reversed by upregulation of hsa-miR-3936. TTC39A-AS1 promoted RNASE3 expression by targeting hsa-miR-3936. Moreover, BBR visibly inhibited the expressions of TTC39A-AS1 and RNASE3 and up-regulated hsa-miR-3936. In conclusion, BBR has the potential to alleviate AD by modulating the TTC39A-AS1/hsa-miR-3936/RNASE3 axis.