TY - JOUR
T1 - Participation of cyclooxygenases in cutaneous thermal nociception under non-inflamed and inflamed conditions
AU - Suzuki, M.
AU - Hayashi, I.
AU - Nara, Y.
AU - Kumagai, Y.
AU - Okamoto, H.
AU - Hoka, S.
AU - Majima, M.
N1 - Funding Information:
Acknowledgements. Part of this work was supported by Academic Frontier Project from the Japanese Ministry of Education, Science, Sports and Culture (to M.M.), grants from Integrative Research Program of the Graduate School of Medical Sciences, Kitasato University (to I.H. and M.M.). Authors thank to Mr. Tomio Hagiwara, the Experimental Animal Center for taking care of experimental animals.
PY - 2001
Y1 - 2001
N2 - Objective and Design: Effects of cyclooxygenase inhibitors on noxious thermal stimuli were investigated in non-inflamed and inflamed rats. Materials: Male Sprague-Dawley rats were used in this study. Treatment: Cyclooxygenase inhibitors, indomethacin, mofezolac, NS-398, and JTE-522 were administered orally at a dose of 10 mg/kg 1 h prior to and 4 h after the intravenous injection of lipopolysaccharide (1 mg/kg). Methods: The nociceptive response was evaluated from the escape latency of foot withdrawal to the thermal stimuli with a beam of light. Expression of cyclooxygenase was examined by reverse transcription-polymerase chain reaction. Results: In normal rat, administration of indomethacin, relatively cyclooxygenase-1-selective inhibitor, mofezolac, or cyclooxygenase-2-selective inhibitors, NS-398 and JTE-522 had no effects on the escape latency against thermal stimuli. Injection of lipopolysaccharide into rat induced the expression of mRNA for cyclooxygenase-2 in the subcutaneous tissue of foot pad. The escape latency at 8 h was significantly shortened by the injection. This hyperalgesia could be reversed by pretreatment of rat with NS-398 or JTE-522, but not with mofezolac. Conclusions: Cyclooxygenases may have little participation in peripheral skin thermal nociception in non-inflamed condition, although cyclooxygenase-2 could be responsible for the hyperalgesia during inflammation induced by lipopolysaccharide.
AB - Objective and Design: Effects of cyclooxygenase inhibitors on noxious thermal stimuli were investigated in non-inflamed and inflamed rats. Materials: Male Sprague-Dawley rats were used in this study. Treatment: Cyclooxygenase inhibitors, indomethacin, mofezolac, NS-398, and JTE-522 were administered orally at a dose of 10 mg/kg 1 h prior to and 4 h after the intravenous injection of lipopolysaccharide (1 mg/kg). Methods: The nociceptive response was evaluated from the escape latency of foot withdrawal to the thermal stimuli with a beam of light. Expression of cyclooxygenase was examined by reverse transcription-polymerase chain reaction. Results: In normal rat, administration of indomethacin, relatively cyclooxygenase-1-selective inhibitor, mofezolac, or cyclooxygenase-2-selective inhibitors, NS-398 and JTE-522 had no effects on the escape latency against thermal stimuli. Injection of lipopolysaccharide into rat induced the expression of mRNA for cyclooxygenase-2 in the subcutaneous tissue of foot pad. The escape latency at 8 h was significantly shortened by the injection. This hyperalgesia could be reversed by pretreatment of rat with NS-398 or JTE-522, but not with mofezolac. Conclusions: Cyclooxygenases may have little participation in peripheral skin thermal nociception in non-inflamed condition, although cyclooxygenase-2 could be responsible for the hyperalgesia during inflammation induced by lipopolysaccharide.
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U2 - 10.1007/s000110050755
DO - 10.1007/s000110050755
M3 - Article
C2 - 11409492
AN - SCOPUS:0034999954
SN - 1023-3830
VL - 50
SP - 283
EP - 287
JO - Inflammation Research
JF - Inflammation Research
IS - 5
ER -