Figure 3.

Cgp91ds‐TAT markedly reduces viral mRNA expression and ROS generation. WT C57Bl/6J mice (8–12 weeks) were treated daily via intranasal administration of Cgp91ds‐TAT (0.2 mg/kg) or DMSO (2%) control. Mice were intranasally infected with PR8 (500 PFU) or PBS control 1 day post initial drug treatment. (A) Quantitative PCR analysis in lung tissue of mRNA from the gene encoding polymerase of influenza virus strain PR8; results were presented relative to those of GAPDH mRNA. (B) BALF was collected for PDB (10⁻⁶ M)‐stimulated ROS production that was quantified by L‐O12 enhanced chemiluminescence. Data were expressed as mean ± SEM (control, n = 7; Cgp91ds‐TAT, n = 5; PR8, n = 9; PR8 + Cgp91ds‐TAT, n = 10). Statistical analysis was conducted using one‐way ANOVA test followed by Tukey's post hoc test for multiple comparison. Statistical significance was taken where P < 0.05. *P < 0.05; **P < 0.01; ***P < 0.001. ANOVA, analysis of variance; BALF, bronchoalveloar lavage fluid; Cgp91ds‐TAT, cholestanol‐conjugated gp91ds‐TAT; DMSO, dimethyl sulphoxide; PCR, polymerase chain reaction; PDB, phorbol dibutyrate; PFU, plaque forming units; RLU, relative light units; ROS, reactive oxygen species; WT, wild type.