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Possible Participation of Nitric Oxide/Cyclic Guanosine Monophosphate/Protein Kinase C/ATP‐Sensitive K + Channels Pathway in the Systemic Antinociception of Flavokawin B
Author(s) -
Mohamad Azam Shah,
Akhtar Muhammad Nadeem,
Khalivulla Shaik Ibrahim,
Perimal Enoch Kumar,
Khalid Mohamed Hanief,
Ong Hui Ming,
Zareen Seema,
Akira Ahmad,
Israf Daud Ahmad,
Lajis Nordin,
Sulaiman Mohd Roslan
Publication year - 2011
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2010.00670.x
Subject(s) - chemistry , protein kinase c , glibenclamide , cyclic guanosine monophosphate , pharmacology , nitric oxide , protein kinase a , nitric oxide synthase , guanosine , phorbol , kinase , biochemistry , endocrinology , medicine , organic chemistry , diabetes mellitus
The possible mechanisms of action in the antinociceptive activity induced by systemic administration (intraperitoneal, i.p.) of flavokawin B (FKB) were analysed using chemical models of nociception in mice. It was demonstrated that i.p. administration of FKB to the mice at 0.3, 1.0, 3.0 and 10 mg/kg produced significant dose‐related reduction in the number of abdominal constrictions. The antinociception induced by FKB in the acetic acid test was significantly attenuated by i.p. pre‐treatment of mice with l‐ arginine, the substrate for nitric oxide synthase or glibenclamide, the ATP‐sensitive K + channel inhibitor, but was enhanced by methylene blue, the non‐specific guanylyl cyclase inhibitor. FKB also produced dose‐dependent inhibition of licking response caused by intraplantar injection of phorbol 12‐myristate 13‐acetate, a protein kinase C activator (PKC). Together, these data indicate that the NO/cyclic guanosine monophosphate/PKC/ATP‐sensitive K + channel pathway possibly participated in the antinociceptive action induced by FKB.