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Fig. 8 | Molecular Medicine

Fig. 8

From: Clara cell 16 KDa protein mitigates house dust mite-induced airway inflammation and damage via regulating airway epithelial cell apoptosis in a manner dependent on HMGB1-mediated signaling inhibition

Fig. 8

CC16 modulates airway epithelial cell apoptosis in response to HDM through the inhibition of HMGB1-mediated signaling. BEAS-2B cells were transfected with pcDNA3.1-HMGB1 plasmid or pcDNA3.1-vector, and then treated with HDM or CC16 or HDM + CC16 for 48 h respectively. a Flow cytometry analysis of HDM-induced apoptosis in BEAS-2B cells. b Western Blotting analysis of HMGB1, TLR4, NF-κB, p-NF-κB, Bcl-2, Bax in BEAS-2B cells under different experiments. c Quantification of the indicated proteins normalized to GAPDH were shown as bar graphs. d Flow cytometry detection of caspase-3 activation in BEAS-2B cells. &p < 0.05 vs. PBS + pcDNA3.1-vector group (control group); &&p < 0.01 vs. control group; #p < 0.05 vs. HDM + pcDNA3.1-vector group; ##p < 0.01 vs. HDM + pcDNA3.1-vector group; *p < 0.05 vs. HDM + CC16 + pcDNA3.1-vector group; **p < 0.01 vs HDM + CC16 + pc DNA3.1-vector group

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