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Fig. 5 | Journal of Inflammation

Fig. 5

From: Cigarette smoke extract-mediated FABP4 upregulation suppresses viability and induces apoptosis, inflammation and oxidative stress of bronchial epithelial cells by activating p38 MAPK/MK2 signaling pathway

Fig. 5

CS-induced 16HBE cell inflammatory response and apoptosis are generated by FABP4-mediated activation of p38 MAPK/MK2 signaling pathway. A CCK-8 assay showed that shRNA-mediated FABP4 ablation rescued the CSE-mediated cell viability decline, (B-C) TUNEL assay showed that shRNA-mediated FABP4 inhibition downregulated the CSE-mediated cell apoptosis (TUNEL positive cells/DAPI positive cells; TUNEL, green; DAPI, blue; Scale bar, 100 µm), (D) ELISA assay showed that shRNA-mediated FABP4 abrogation alleviated the CSE-mediated cellular inflammatory response (TNF-α, IL-1β and IL-6), (E) Western blot analysis showed that shRNA-mediated FABP4 abolition downregulated the CSE-mediated Cox-2 and iNOS protein levels, which were all significantly reversed after treatment with 30 μM asiatic acid, an agonist of p38 MAPK at 37 °C for 1 h. The normal 16HBE cells without transfection and CSE or asiatic acid treatment were used as control. ***p < 0.001 vs. control group; #p < 0.05, ##p < 0.01, ###p < 0.001 vs. 2% CSE + shRNA-FABP4-1 group. 16HBE, Human bronchial epithelioid cell line; FABP4, Fatty Acid Binding Protein 4; GAPDH, Glyceraldehyde-3-Phosphate Dehydrogenase; CSE, cigarette smoke extract; TNF-α, Tumor Necrosis Factor α; IL-1β, Interleukin 1 Beta; IL-6, Interleukin 6; Cox-2, Prostaglandin-Endoperoxide Synthase 2; iNOS, Nitric Oxide Synthase 2

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