Fig. 6

SN50 and TLR4 homozygous knockout inhibited endotoxin-exacerbated mechanical ventilation-induced NF-κB activation and TLR4 expression. a, b, and c Western blots were conducted using antibodies that recognize the expression levels of phosphorylated NF-κB and IκBα and antibodies that recognize the expression levels of total NF-κB, IκBα, TRL4, and GAPDH from the diaphragms of nonventilated control mice and mice ventilated at a tidal volume of 6 mL/kg or 10 mL/kg for 8 h with or without LPS administration (n = 5 per group). Arbitrary units were expressed as relative NF-κB and TLR4 expression (n = 5 per group). d Representative micrographs (×400) with TRL4 staining of paraffin diaphragm sections and quantification were from the diaphragms of nonventilated control mice and mice ventilated at a tidal volume of 6 mL/kg or 10 mL/kg for 8 h with or without LPS administration (n = 5 per group). SN-50 2 mg/kg was given intraperitoneally 30 min before ventilation. A dark-brown diaminobenzidine signal identified by arrows indicates positive staining for TRL4 in the diaphragm, whereas shades of bluish tan signify nonreactive cells. *P < 0.05 versus the nonventilated control mice with LPS treatment; ^†P < 0.05 versus all other groups. Scale bars represent 20 μm. Inhibitor-κBα IκBα, TLR4^−/− TLR4-deficient mice