Figure 3
Inhibition of airway inflammation by the KG3P and nepetin in a CFD-induced murine model of airway inflammation. (A) Scheme for the CFD sensitization and challenge protocol. Mice were exposed to 100 μL of CFD [Coal (5 mg/mL), Fly ash (10 mg/mL), Diesel exhaust particles (DEP, 5 mg/mL)] mixed solution by intranasal tracheal injection thrice in 3 day intervals for 12 days. (B, C) KG3P and nepetin inhibited asymmetric dimethyl-arginine (ADMA) and symmetric dimethly-arginine (SDMA) production in serum obtained from CFD mice by ELISA kit. (D) Effect of KG3P and nepetin treatment on lung histopathology in CFD-CTL mice as visualized by H&E and Masson’s Trichrome staining. . Representative sections from each treatment group are shown. (a) BALB/c normal Wild type control (WT), (b) CFD-sensitized control mice (CTL), (c) 10 mg/kg montelukast-treated CFD-sensitized mice, (d) 200 mg/kg KG3P-treated CFD-sensitized mice, (e) 100 mg/kg KG3P-treated CFD-sensitized mice, and (f) 20 mg/kg nepetin-treated CFD-sensitized mice. M–T staining pictures have the same order for groups in H&E staining (g–l). (E) Quantitative analyses of the degree of lung tissue damage in the sections. Data are from individual mice, with arithmetic mean points shown in histograms. Values are expressed as mean ± SEM (n = 8 mice). #p < 0.05, ##p < 0.01, and ###p < 0.001 (compared to WT), and *p < 0.05, **p < 0.01, and ***p < 0.001 (compared to CTL).
