title: Effect of etodolac, a COX-2 inhibitor, on neuropathic pain in a rat model.
abstract: Etodolac, a cyclooxygenase-2 inhibitor, may alleviate nociceptive pain and inhibit the activation of osteoclasts. The aim of the present study was to determine whether etodolac can alleviate heat-evoked hyperalgesia and investigate its possible protective effects on osteoporosis induced by chronic constriction injury (CCI) in rats. A CCI to the sciatic nerve was performed, after which the rats received etodolac orally in a volume of 2 ml at 0, 1, and 10 mg/kg/day for 1 to 5 weeks following surgery (experiment 1); at 0 and 10 mg/kg/day for 1 day to 5 weeks following surgery (experiment 2); and at 0 mg/kg/day for 1 to 5 weeks, 10 mg/kg/day for 1 to 2 weeks after surgery, or 10 mg/kg/day for 1 to 3 weeks after surgery (experiment 3). Paw withdrawal latency after exposure to heat, bone mineral content (BMC) and bone mineral density (BMD) in the whole tibial bone, and the number of tartrate resistant acid phosphate (TRAP)-positive multinucleated osteoclasts were measured. Etodolac alleviated heat-evoked hyperalgesia in the CCI rats and the increase in number of TRAP-positive multinucleated osteoclasts on the CCI-side was abrogated, however, it did not inhibit the decrease of BMC and BMD on the CCI-side. Our results suggest that etodolac is useful for treatment of neuropathic pain.
authors.affiliation: Department of Anesthesiology and Critical Care, Division of Clinical Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami, Hiroshima 734-8551, Japan. h.suyama@ccv.ne.jp
authors.forename: Hidemichi
authors.initials: H
authors.lastname: Suyama
authors.forename: Masashi
authors.initials: M
authors.lastname: Kawamoto
authors.forename: Syafruddin
authors.initials: S
authors.lastname: Gaus
authors.forename: Osafumi
authors.initials: O
authors.lastname: Yuge
mesh_terms: D000135:Acid Phosphatase / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D015519:Bone Density / Q000187:drug effects / Q000502:physiology; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004195:Disease Models, Animal; D017308:Etodolac / Q000494:pharmacology*; D006930:Hyperalgesia / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D007527:Isoenzymes / Q000037:antagonists & inhibitors* / Q000187:drug effects / Q000378:metabolism; D008026:Ligation; D009437:Neuralgia / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D010010:Osteoclasts / Q000187:drug effects / Q000378:metabolism; D010024:Osteoporosis / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D010147:Pain Measurement; D010525:Peripheral Nerves / Q000187:drug effects* / Q000378:metabolism; D010523:Peripheral Nervous System Diseases / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D020426:Sciatic Neuropathy / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D000071681:Tartrate-Resistant Acid Phosphatase; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D017308:Etodolac; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase