Anti-hyperalgesic effect of a benzilidine-cyclohexanone analogue on a mouse model of chronic constriction injury-induced neuropathic pain: Participation of the κ-opioid receptor and KATP
| Autor: | Daud Ahmad Israf Ali, Lee Ming-Tatt, Muhammad Nadeem Akhtar, Shaik Ibrahim Khalivulla, Nordin H. Lajis, Mohd Roslan Sulaiman, Enoch Kumar Perimal, Ahmad Akira |
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| Rok vydání: | 2013 |
| Předmět: |
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ATP-sensitive potassium channel medicine.drug_class Clinical Biochemistry (+)-Naloxone Pharmacology Toxicology Biochemistry Benzylidene Compounds Nitric oxide Behavioral Neuroscience chemistry.chemical_compound Mice KATP Channels Opioid receptor Naltrindole medicine Animals Cyclic guanosine monophosphate Biological Psychiatry Mice Inbred BALB C Chemistry Cyclohexanones Receptors Opioid kappa Potassium channel blocker Disease Models Animal Neuropathic pain Neuralgia medicine.drug Signal Transduction |
| Zdroj: | Pharmacology, biochemistry, and behavior. |
| ISSN: | 1873-5177 |
| Popis: | The present study investigated the analgesic effect of a novel synthetic cyclohexanone derivative, 2,6-bis-4-(hydroxyl-3-methoxybenzilidine)-cyclohexanone or BHMC in a mouse model of chronic constriction injury-induced neuropathic pain. It was demonstrated that intraperitoneal administration of BHMC (0.03, 0.1, 0.3 and 1.0mg/kg) exhibited dose-dependent inhibition of chronic constriction injury-induced neuropathic pain in mice, when evaluated using Randall-Selitto mechanical analgesiometer. It was also demonstrated that pretreatment of naloxone (non-selective opioid receptor blocker), nor-binaltorphimine (nor-BNI, selective κ-opioid receptor blocker), but not β-funaltrexamine (β-FN, selective μ-opioid receptor blocker) and naltrindole hydrochloride (NTI, selective δ-opioid receptor blocker), reversed the anti-nociceptive effect of BHMC. In addition, the analgesic effect of BHMC was also reverted by pretreatment of 1H-[1,2,4]Oxadiazole[4,3-a]quinoxalin-1-one (ODQ, soluble guanosyl cyclase blocker) and glibenclamide (ATP-sensitive potassium channel blocker) but not Nω-nitro-l-arginine (l-NAME, a nitric oxide synthase blocker). Taken together, the present study demonstrated that the systemic administration of BHMC attenuated chronic constriction, injury-induced neuropathic pain. We also suggested that the possible mechanisms include κ-opioid receptor activation and nitric oxide-independent cyclic guanosine monophosphate activation of ATP-sensitive potassium channel opening. |
| Databáze: | OpenAIRE |
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