Table 1.

Percentage inhibition of the peak ACTH response to local inflammation and electrofootshock stress produced by either anti-TNF-α or rhTNFR:Fc

	Intravenous route	Intracerebroventricular route
Local inflammation
Immunoneutralization
Anti-TNF-α	25  ± 8	64  ± 101-165
Soluble receptor construct
1 μg rhTNFR:Fc	29  ± 19	62  ± 6ns
10 μg rhTNFR:Fc	4  ± 13	65  ± 111-160
50 μg rhTNFR:Fc	22  ± 20	72  ± 8*
Footshock stress
Immunoneutralization
Anti-TNF-α	Not done	−1  ± 14ns

Values represent the mean ± SEM of the % inhibition of the peak ACTH response to local inflammation induced by either turpentine (7.5 h) or electrofootshock (30 min); 100% response was calculated as the difference between the mean plasma ACTH concentrations observed in control, unstimulated rats and those in NRS- or PBS-pretreated turpentine or NRS-pretreated electrofootshock rats, as appropriate. The ACTH “response” in individual, treated (anti-TNF-α or rhTNFR:Fc) rats was then similarly calculated, and the % inhibition was determined for each animal. ns, Not significant;

^*p < 0.05,

F1-160: p < 0.01,

F1-165: p < 0.001 versus respective intravenous treatment (unpaired Student’s t test).