B. Safiehgarabedian et al., INVOLVEMENT OF INTERLEUKIN-1-BETA, NERVE GROWTH-FACTOR AND PROSTAGLANDIN E-2 IN ENDOTOXIN-INDUCED LOCALIZED INFLAMMATORY HYPERALGESIA, British Journal of Pharmacology, 121(8), 1997, pp. 1619-1626
1 Intraplantar endotoxin (ET) injection (1.25 mu g) into the hind paw
of rats resulted in a localized inflammatory hyperalgesia, as assessed
by paw pressure (PP), paw immersion (PI), tail flick (TF) and hot pla
te (HP) tests. 2 ET injection resulted in a significant elevation in t
he levels of interleukin-1 beta (IL-1 beta) and nerve growth factor (N
GF) in the injected foot as compared with the non-injected foot. This
increase was attenuated by intraperitoneal injections of dexamethasone
(200 and 400 mu g kg(-1)) and to a lesser extent by indomethacin (2 a
nd 8 mg kg(-1)). 3 The tripeptide Lys-D-Pro-Val, which is known to ant
agonize IL-1 beta and prostaglandin E-2 (PGE(2)) reversed mechanical h
yperalgesia, as assessed by the PP test, and reduced significantly the
rmal hyperalgesia, as assessed by the HP and TF tests. 4 IL-1ra revers
ed both mechanical (PP) and thermal (PI) nociceptive thresholds tested
on the injected leg and significantly reduced thermal hyperalgesia, a
s assessed by the HP and TF tests. 5 A sheep, anti-mouse NGF antiserum
reversed mechanical hyperalgesia (PP test) but had little or no effec
t on thermal hyperalgesia (PI, HP and TF tests). 6 Our results indicat
e the importance of IL-1 beta, NGF and prostaglandin E-2 (PGE(2)) in t
he development of ET induced hyperalgesia and the possible existence o
f different mechanisms underlying thermal and mechanical as well as ce
ntral and peripheral hyperalgesia.