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Fig. 2 | Journal of Inflammation

Fig. 2

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. 2

CS-induced 16HBE cell apoptosis is alleviated by shRNA-mediated FABP4 abrogation. A, B The knockdown efficiency in 16HBE cells treated with 2% CSE was tested by the western blot analysis and qRT-PCR analysis. GAPDH served as the loading control. C CCK-8 assay showed a rescue of CSE-mediated cell viability decrease in 16HBE cells transfected with shRNA-FABP4-1 as compared with the cells transfected with shRNA-NC. D TUNEL assay showed a downregulation of CSE-mediated cell apoptosis (TUNEL positive cells/DAPI positive cells; TUNEL, green; DAPI, blue; Scale bar, 100 µm) 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 < 0.05, ###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

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Journal of Inflammation

ISSN: 1476-9255

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