Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

Abstract

Background/aim Pressure ulcers are a disastrous health issue in which inflammation is involved. Emodin possesses biological properties in inflammation. Our study investigated functions of emodin in lipopolysaccharide (LPS)-treated HaCaT cells.Methods LPS was used to induce cell inflammation. MTT and flow cytometry were applied for cell viability and apoptosis assays, respectively. Moreover, apoptotic proteins were detected by western blot. Similarly, inflammatory factors and signalling related proteins were also determined by western blot.Results Emodin increased cell viability and diminished apoptosis in LPS-treated HaCaT cells. Moreover, cleaved-PARP, cleaved-caspase-3 and cleaved-caspase-9 were all downregulated by emodin. Furthermore, inflammatory factors IL-1β, IL-6, Cox-2 and iNOS were inhibited by emodin in LPS-treated cells. In addition, emodin decreased phosphorylation of p65 and IκBα and the level of PTEN while enhanced phosphorylation of PI3K and AKT. Importantly, emodin increased expression of miR-21 suppressed by LPS and miR-21 downregulation negated the protective functions of emodin.Conclusions Emodin promoted cell growth presented by increasing viability and blocking apoptosis process with inflammation inhibition. The protective activity of emodin was mediated by miR-21 up-regulation.

Keywords

• Pressure ulcers
• inflammation
• NF-κB
• PTEN/PI3K/AKT