Potential of Inducible Nitric Oxide Synthase as a Therapeutic Target for Allergen-Induced Airway Hyperresponsiveness: A Critical Connection to Nitric Oxide Levels and PARP Activity

Figure 3

Effect of iNOS inhibition by L-NIL on AHR manifestation upon exposure to HDM in mice and the influence of NO supplementation by nitrite administration. C57BL/6 mice were subjected to HDM sensitization followed by acute (a) or chronic (b) intranasal challenge with HDM or were left unchallenged. Challenged mice were administered i.p. 5 mg/kg L-NIL with or without 20 mg/kg of nitrite (NaNO₂) as NO source 30 min after each HDM challenge. Penh was recorded 24 h after the last HDM challenge using a whole body plethysmograph before and after the indicated concentrations of aerosolized MeCh. Results are plotted as maximal fold increase of Penh relative to baseline and expressed as mean ± SEM, where mice per group. and , difference from HDM challenged mice with and , respectively; , difference from control unchallenged mice with . RNA isolated from the lungs of the different experimental groups was reverse-transcribed and the resulting cDNA was subjected to real-time PCR with primer sets specific to mouse IL-5 or β-actin. Data is expressed as fold change of values detected in lungs of control mice. , difference from control unchallenged mice with ; , difference from HDM-exposed mice receiving L-NIL with . ns, nonsignificant difference with .

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