Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 283-287 |
| Number of pages | 5 |
| Journal | Inflammation Research |
| Volume | 50 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - May 29 2001 |
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All Science Journal Classification (ASJC) codes
- Immunology
- Pharmacology
Cite this
Participation of cyclooxygenases in cutaneous thermal nociception under non-inflamed and inflamed conditions. / Suzuki, M.; Hayashi, I.; Nara, Y.; Kumagai, Y.; Okamoto, H.; Hoka, Sumio; Majima, M.
In: Inflammation Research, Vol. 50, No. 5, 29.05.2001, p. 283-287.Research output: Contribution to journal › Article
}
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, Sumio
AU - Majima, M.
PY - 2001/5/29
Y1 - 2001/5/29
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
VL - 50
SP - 283
EP - 287
JO - Inflammation Research
JF - Inflammation Research
SN - 1023-3830
IS - 5
ER -