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Fig. 6 | Molecular Medicine

Fig. 6

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. 6

HMGB1 drives airway epithelial cell apoptosis through TLR4/NF-κB signal pathway in HDM conditions. BEAS-2B cells were transfected with si-NC or si-HMGB1, and then incubated in the presence or absence of HDM stimulation. a Cell viability of si-NC or si-HMGB1 transfected BEAS-2B cells was assessed by CCK-8 assay after HDM stimulation for 12, 24, 48 h respectively. b The percentages of apoptosis cells were measured by flow cytometry. c Expressions of HMGB1, TLR4, NF-κB, p-NF-κB, Bcl-2, Bax and cleaved caspase-3 were analyzed by Western Blotting analysis. The level of β-actin served as a loading control. d Grey values of the indicated proteins were quantified by densitometric analysis. e The percentages of cleaved caspase-3 positive cells by flow cytometry. Data are shown as mean ± SEM. #p < 0.05 vs. PBS + si-NC group (control group); ##p < 0.01 vs. PBS + si-NC group (control group); *p < 0.05 vs. HDM + si-NC group; **p < 0.01 vs. HDM + si-HMGB1 group

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Molecular Medicine

ISSN: 1528-3658