Antinociceptive Activities of the Methanolic Extract of the Stem Bark of Boswellia dalzielii Hutch. (Burseraceae) in Rats Are NO/cGMP/ATP-Sensitive-K+ Channel Activation Dependent. (6th December 2017)

• Record Type: Journal Article
• Authors: Mbiantcha, Marius; Ngouonpe Wembe, Alain; Dawe, Amadou; Yousseu Nana, William; Ateufack, Gilbert
• Other Names: Capasso Raffaele Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2017(2017)
• Publication Date: 2017-12-06
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2017/6374907
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : Boswellia dalzielii (B. dalzielii) is traditionally used in the treatment of rheumatism, pain, and inflammation. The present investigation evaluates the property and possible mechanism of action of the methanolic extract of B. dalzielii (BDME) on inflammatory and neuropathic pain models. Effects of BDME (250 and 500 mg/kg), orally administered, were verified in mechanical hypernociception induced by LPS or PGE2 . Mechanical hyperalgesia, cold allodynia, and heat hyperalgesia were used in vincristine-induced neuropathic pain. NW-nitro-L-arginine methyl ester (inhibitor of nitric oxide synthase), glibenclamide (ATP-sensitive potassium channel blocker), methylene blue (cGMP blocker), or naloxone (opioid antagonist receptor) has been used to evaluate the therapeutic effects of BDME on PGE2 -induced hyperalgesia. Chemical profile of BDME was determined by using HPLC-XESI-PDA/MS. BDME showed significant antinociceptive effects in inflammatory pain caused by LPS and PGE2 . The extract also significantly inhibited neuropathic pain induced by vincristine. The antinociceptive property of BDME in PGE2 model was significantly blocked by L-NAME, glibenclamide, methylene blue, or naloxone. The present work reveals the antinociceptive activities of BDME both in inflammatory and in neuropathic models of pain. This plant extract may be acting firstly by binding to opioid receptors and secondly by activating the NO/cGMP/ATP-sensitive-K + channel pathway.