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Fig. 7 | Molecular Medicine

Fig. 7

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. 7

HMGB1 overexpression abolishes the protective effect of CC16 against HDM-induce airway damage. HMGB1 overexpression in mouse lungs was induced by intratracheally injection of Ad-HMGB1 vector. Ad-GFP was used as the negative control as shown in Fig. 5. Then the gene-modified mice was sensitized and challenged by HDM with or without CC16 (10 g/g) administration. a Relative mRNA levels of HMGB1 in mouse lungs from different groups. b Representative images of lung tissues showed airway wall thickening, mucous hyperplasia and collagen deposition. c The caspase-3 activities of the lungs in different treatment groups. Data are expressed as &&p < 0.01 vs. control + Ad-GFP group; #p < 0.05 vs. HDM + Ad-GFP group; ##p < 0.01 vs. HDM + Ad-GFP group; *p < 0.05 vs. HDM + Ad-HMGB1 + CC16 group; **p < 0.01 vs. HDM + Ad-HMGB1 + CC16 group

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Molecular Medicine

ISSN: 1528-3658