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Fig. 1 | Journal of Inflammation

Fig. 1

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. 1

CS mediates the up-regulation of FABP4 in 16HBE cells. A 16HBE cells were treated with different doses of CSE (0.5%, 1%, 2% and 4%) for 24 h, and the normal 16HBE cells without CSE treatment were used as control. Representative Western blot images and quantitative analysis, using the rabbit anti-FABP4, showed an incremental increase in the FABP4 expression with CSE. GAPDH served as the loading control. B qRT-PCR analysis, using the primer of human FABP4, showed the experimental results consistent with (A). **p < 0.01, ***p < 0.001 vs. control group. C 16HBE cells were treated with 2% CSE for different time (0 h, 12 h, 24 h, 36 h and 48 h). 2% CSE treatment increased the FABP4 expression in a time dependent manner with a maximum expression at 48 h after the 2% CSE treatment. GAPDH served as the loading control. D qRT-PCR analysis, using the primer of human FABP4, showed the experimental results consistent with (C). ***p < 0.001 vs. 0 h 2% CSE 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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