RETRACTED: Schizandrin A Alleviates LPS-Induced Injury in Human Keratinocyte Cell Hacat Through a MicroRNA-127-Dependent Regulation (Publication with Expression of Concern. See vol. 55, pg. 536, 2021) (Retracted Article)

Background/Aims: Inflammatory skin diseases are the most common problems in dermatology. Schizandrin A (SchA) has been reported to have anti-inflammatory properties. Herein, we aimed to investigate the protective effects of SchA on lipopolysaccharide (LPS)-induced injury in keratinocyte HaCaT cells. Methods: Inflammation injury in HaCaT cells was induced by LPS treatment. Cell viability, apoptotic cell rate, and apoptosis-related proteins were analyzed by cell counting kit-8 (CCK-8) assay, Annexin V-(fluorescein isothiocyanate (FITC)/ Propidium Iodide (PI) double staining method, and western blot, respectively. The pro-inflammatory factors were analyzed by western blot and quantified by enzyme linked immunosorbent assay (ELISA). Expression of miR-127 in SchA-treated cells was analyzed by qRT-PCR. The effects of SchA on activations of p38MAPK/ERK and JNK pathways were analyzed by western blot. Results: SchA protected HaCaT cells from LPS-induced inflammation damage via promoting cell viability, suppressing apoptosis. Meanwhile, SchA inhibited IL-1 beta, IL-6, and TNF-alpha expression. miR-127 expression was up-regulated in LPS-treated HaCaT cells but down-regulated after SchA treatment. Overexpression of miR-127 inhibited cell growth and induced expression of IL-1 beta, IL-6 and TNF-alpha. Additionally, miR-127 overexpression impaired the protective effects of SchA, implying mi R-127 might be correlated to the anti-inflammation property of SchA and also involved in inactivation of p38MAPK/ERK and JNK pathways by SchA. Conclusion: miR-127 is involved in the protective functions of SchA on LPS-induced inflammation injury in human keratinocyte cell HaCaT, which might inactivates of p38MAPK/ERK and JNK signaling pathways in HaCaT cells. (C) 2018 The Author(s) Published by S. Karger AG, Basel