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. 2018 Dec 28;20(1):105. doi: 10.3390/ijms20010105

Figure 1.

Figure 1

Secretion of VEGF from HCtAEC in response to SAA in the absence and presence of the NFκB inhibitor BAY11-7082. HCtAEC were pre-incubated (1.5 h) with 0, 1, 10 or 100 μM BAY11-7082 or vehicle (control) then treated with 10 μg/mL SAA. After 4.5 h the levels of secretory VEGF in cell supernatants was assessed by commercial ELISA assays. Data were expressed as a fold-change compared to control cells. Data represents the mean ± SD (n = 4 individual experiments, each performed in duplicate; therefore, data represent 4 technical replicates). * p < 0.05 compared to control cells. All data was normalised to the corresponding level of cell confluence (expressed as a percentage %) determined using an IncuCyte system immediately prior to cell harvest for ELISA. This approach to normalizing data was necessary as there was some level of toxicity for BAY11-7082 particularly at the higher doses of inhibitor tested.