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. 2021 Jul 26;22(4):1059. doi: 10.3892/etm.2021.10493

Figure 6.

Figure 6

miR-139-5p overexpression inhibits LPS-induced inflammation and oxidative stress via targeting ROCK1 in NHBEs. NHBEs were divided into six groups: Control, LPS, LPS plus miR-NC mimics, LPS plus miR-139-5p mimics, LPS plus miR-139-5p mimics and empty vector, and LPS plus miR-139-5p mimics and Ov-ROCK1. (A) Relative mRNA expressions of MUC5AC and MUC1 were measured using RT-qPCR. (B) Proinflammatory cytokine levels in the treated NHBEs were examined using ELISA. (C) ROS levels in different groups. (D) Expression levels of NLRP3, ASC and caspase-1 in the treated NHBEs were examined using western blotting. (E) SOD, GSH-px and LDH activities and MDA levels were determined using commercial assay kits. Data are presented as the mean ± standard deviation. ***P<0.001 vs. control; #P<0.01, ##P<0.005 and ###P<0.001 vs. miR-NC; ΔΔP<0.005 and ΔΔΔP<0.001 vs. miR-139-5p mimics + Vector. ROCK1, Rho-associated kinase 1; miR, microRNA; RT-qPCR, reverse transcription-quantitative PCR; NHBEs, normal human bronchial epithelial cells; Ov, overexpression; SOD, superoxide dismutase; MDA, malondialdehyde; LDH, lactate dehydrogenase; GSH-px, glutathione peroxidase; LPS, lipopolysaccharide; NC, negative control; MUC, mucin; NLRP3, NLR family pyrin domain containing 3; ASC, apoptosis-associated speck-like protein containing a CARD.