Effects of the inhibitory peptide of polysaccharide binding protein on the NF-κB activity of mouse lung tissues induced by LPS in a mouse model with endotoxemia

To investigate the in vivo effects of a inhibitory peptide P12 of polysaccharide binding protein(LBP) on the activity of nuclear factor κB(NF-κB) in a mouse model with endotoxemia,40 mice of Kunming strain were randomly divided into 5 groups,i.e.control group,endotoxemia group,treated group with low-dose of P12,treated group with middle dose of P12 and treated group with high dose of P12,in which the endotoxemia group of mice was established by intraperitoneal injections of LPS and in the treated groups of mice,P12 was instilled through tail veins.The activity of NF-κB was evaluated by immunochemical staining,image analysis and Western blotting and the production of nitric oxide was measured by enzymatic assay with nitrate reductase.It was demonstrated that the P65 subunit of NF-κB entered into nuclei after stimulation with LPS,and the Absorbance ratio of the P65 subunit in the nucleus and cytoplasm of the treated groups of mice with low-,middle and high-dose of P12 were 1.24±0.34,1.45±0.53 and 0.84±0.75 respectively,all lowering to that of the LPS-treated group(3.08±0.16).The concentrations of NO in sera of the treated groups with low-,middle-and high-dose of P12 were(106.17±24.93) μmol/L,(80.84±19.32) μmol/L and(67.28±16.67) μmol/L respectively,which were all lower than that of mice with endotoxemia(185.49±20.13) μmol/L.It is evident that the inhibitory peptide P12 can inhibit the activation of NF-κB in lung tissues of mice with endotoxemia induced by LPS and reduce the release of NO,indicating its potential preventive and early therapeutic effects on endotoxemia.