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Fig. 3 | Journal of Inflammation

Fig. 3

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. 3

CS-induced 16HBE cell inflammatory response was reduced by shRNA-mediated FABP4 elimination. A ELISA assay showed an alleviation of CSE-mediated promotion of TNF-α, IL-1β and IL-6 levels in 16HBE cells transfected with shRNA-FABP4-1 as compared with the cells transfected with shRNA-NC. B Western blot analysis showed a downregulation of CSE-mediated increase of Cox-2 and iNOS protein levels in 16HBE cells transfected with shRNA-FABP4-1 as compared with the cells transfected with shRNA-NC. The normal 16HBE cells without transfection and CSE treatment were used as control. ***p < 0.001 vs. control group; ###p < 0.001 vs. 2% CSE + shRNA-NC 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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Journal of Inflammation

ISSN: 1476-9255

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