Fig. 6

SNHG16 affected the LPS-mediated lung epithelial cell injury by modulating the miR-128-3p/HMGB3 axis. Normal human lung epithelial cell line BEAS-2B were transfected with SNHG16 overexpression plasmids and/or miR-128-3p mimics and then treated with LPS (100 ng/ml) for 24 h. a MTT assay was performed to examine cell viability; b, c Flow cytometry was employed to monitor apoptosis; d–f The expression of TNF-α, IL-1β, and IL-6 in cells was compared by ELISA; g WB was conducted to compare the levels of the pro-inflammatory proteins NF-κB, MAPK-P38, iNOS and COX2. *P < 0.05; **P < 0.01; ***P < 0.001 (vs. LPS group); ^#P < 0.05; ^##P < 0.01; ^###P < 0.001 (vs. LPS + SNHG16 group). N = 3. All experiments were repeated for three times