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

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Akhtar, Muhammad Nadeem and Shaik Ibrahim, Khalivulla and Lee, Ming-Tatt and Nordin, Lajis and Enoch Kumar, Perimal and Ahmad, Akira and Daud Israf, Ali and Mohd Roslan, Sulaiman (2013) 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. Pharmacology Biochemistry and Behavior, 114-115 . pp. 58-63. ISSN 0091-3057 (print); 1873-5177 (online)

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Official URL: http://dx.doi.org/10.1016/j.pbb.2013.10.019

Abstract

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 1.0 mg/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.

Item Type:Article
Additional Information:Indexed in Scopus, ISI. IF: 2.608
Uncontrolled Keywords:Neuropathic pain; Chronic constriction injury; Opioid receptor; Nitric oxide; Cyclic guanosine monophosphate; ATP-sensitive potassium channel
Subjects:Q Science > QR Microbiology
Divisions:Faculty of Industrial Sciences And Technology
ID Code:5245
Deposited By: Noorul Farina Arifin
Deposited On:31 Mar 2014 16:38
Last Modified:02 Nov 2017 15:18

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