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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: J Immunol. 2013 Jan 25;190(5):2447–2454. doi: 10.4049/jimmunol.1202699

Figure 2. Antioxidants and PAF-AH but not COX-2 inhibitor block CS-exposure generated systemic PAF-R agonists; lack of role for nicotine.

Figure 2

Female mice were placed on 10g/kg vitamin C-enriched chow + 5 mM NAC in water for 10 days vs standard chow/water, or i.p. injections of 5 mg/kg PAF-AH (24 h before CS) or 200 ng of the COX-2 inhibitor NS-398 or vehicle control (2h before CS), or were treated with low-nicotine CS. Groups of 3–4 mice were exsanguinated immediately following 5 h of CS exposure and PAF-R agonistic activity measured as in Fig 1. The data are mean ± SE % maximal (CPAF) response from at least 4 pooled samples. ***Statistically significant (p < 0.001) differences from control CS-treated.