RESUMO
BACKGROUND: Pressure ulcers are a common issue for people who have limited mobility. This study tested the impact of liquiritin on human keratinocyte HaCaT cell inflammatory damage aroused by lipopolysaccharide (LPS). METHODS: HaCaT cells were underwent LPS and/or liquiritin incubation. Cell viability, apoptosis and inflammatory molecules interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and cyclooxygenase-2 (Cox-2) expressions, along with nuclear factor kappa B (NF-κB) and c-Jun N-terminal kinase (JNK) pathways activities were tested by MTT assay, Guava Nexin assay, ELISA and western blotting, respectively. qRT-PCR was done for measuring microRNA-31 (miR-31) expression. miR-31 inhibitor was transfected to silence miR-31. Animal pressure ulcers was established on the dorsal skin of adult rats. The effects of liquiritin on wound healing were analyzed by measuring wound closure rates. RESULTS: LPS aroused HaCaT cell inflammatory damage, as evidenced by the decrease of cell viability, increase of cell apoptosis and enhanced expressions of IL-6, TNF-α and Cox-2. Liquiritin protected HaCaT cells against LPS-aroused inflammatory damage through increasing cell viability, decreasing cell apoptosis, and reducing IL-6, TNF-α and Cox-2 expressions. Liquiritin attenuated the LPS-aroused NF-κB and JNK pathways activation in HaCaT cells. Rat pressure ulcers model also confirmed that liquiritin promoted wound healing. In mechanism, miR-31 expression was boosted by liquiritin in HaCaT cells. Silencing miR-31 weakened the impacts of liquiritin on LPS-irritated HaCaT cells. Myeloid differentiation factor 88 (MyD88) was a target of miR-31 in HaCaT cells. CONCLUSION: This research affirmed the beneficial impact of liquiritin on pressure ulcers. Liquiritin reduced LPS-aroused HaCaT cell inflammatory damage might be implemented via raising miR-31 expression, lowering MyD88 expression, and repressing NF-κB and JNK pathways.
