LAUSR

BACKGROUND Pneumonia is a common respiratory disease in pediatrics. Quercetin is a natural flavonoid widely distributed in many foods and drinks. Herein, we focused our investigation on the possible protective activity of quercetin in lipopolysaccharide (LPS)-caused inflammatory damage of WI-38 lung fibroblasts. METHODS Viability and apoptosis of WI-38 were respectively tested using CCK-8 assay and Annexin V-FITC/PI staining. qRT-PCR was used to measure the expression levels of microRNA-221 (miR-221), IL-6 and TNF-a in WI-38. ELISA was conducted to determine the concentrations of IL-6 and TNF-a in culture supernatant of WI-38. miR-221 mimic was transfected to increase miR-221 expression. The protein levels of key molecules involving in cell apoptosis, inflammation, NF-κB and JNK pathways were assessed using western blotting. RESULTS LPS stimulation caused inflammatory damage of WI-38 lung fibroblasts via suppressing cell viability, inducing cell apoptosis and enhancing the production of inflammatory cytokines IL-6 and TNF-a. Quercetin treatment mitigated the LPS-caused inflammatory damage of WI-38 lung fibroblasts via enhancing cell viability, inhibiting cell apoptosis and reducing the production of inflammatory cytokines IL-6 and TNF-a. Moreover, quercetin ameliorated LPS-caused up-regulation of miR-221 in WI-38. The effects of quercetin on LPS-caused inflammatory damage of WI-38 were reversed by miR-221 overexpression. Furthermore, quercetin inactivated NF-κB and JNK pathways in LPS-treated WI-38 via down-regulation of miR-221. CONCLUSION This research verified the protective effects of quercetin on lung fibroblasts inflammatory damage. We revealed that quercetin ameliorated LPS-caused inflammatory damage of WI-38 lung fibroblasts might be through down-regulation of miR-221 and inactivation of NF-κB and JNK pathways.