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 RESEARCH ARTICLE
Year : 2012  |  Volume : 44  |  Issue : 6  |  Page : 765-773

Analgesic effects of stem bark extracts of Trichilia monadelpha (Thonn.) JJ De Wilde


1 Department of Pharmacology, College of Health Sciences, Kwame Nkrumah University of Science & Technology, Kumasi, Ghana
2 Department of Pharmacology, School of Medicine and Health Sciences, University of Development Studies, Tamale, Ghana

Correspondence Address:
Eric Woode
Department of Pharmacology, College of Health Sciences, Kwame Nkrumah University of Science & Technology, Kumasi
Ghana
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0253-7613.103299

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Objectives: Various parts of Trichilia monadelpha (Thonn) JJ De Wilde (Fam. Meliaceae) are used in Ghanaian traditional medicine for the treatment of painful and inflammatory conditions. The present study examined the analgesic properties of the petroleum ether (PEE), ethyl acetate (EAE), and the hydro-ethanolic (HAE) extract of the stem bark of the plant in murine models. Materials and Methods: PEE, EAE, and HAE were assessed in chemical (acetic acid-induced abdominal writhing and formalin tests), thermal (hot plate test), and mechanical (Randall-Selitto paw pressure test) pain models. The possible mechanisms of the antinociceptive action were also examined with various antagonists in the formalin test. Results: HAE, EAE, and PEE, each at doses of 10-100 mg/kg orally, and the positive controls (morphine and diclofenac) elicited significant dose-dependent antinociceptive activity in the chemical (acetic acid abdominal writhing and formalin tests), thermal (hot plate test), and mechanical (Randall-Selitto paw pressure test) pain models in rodents. The antinociceptive effect of HAE was partly or wholly reversed by systemic administration of atropine, naloxone, and glibenclamide. The antinociceptive effects of EAE and PEE were inhibited by atropine. Conclusion: The extracts HAE, EAE, and PEE caused dose-related antinociception in chemical, thermal, and mechanical models of pain in animals. The mechanism of action of HAE involves an interaction with muscarinic cholinergic, adenosinergic, opioidergic pathways, and ATP-sensitive K + channels while that of EAE and PEE involve the muscarinic cholinergic system.






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