%0 Journal Article
%T Antiallergic and Antiarthritic Effects of Stem Bark Extract of Glyphaea brevis (Spreng) Monachino (Tiliaceae) in Murine Models
%A David D. Obiri
%A Newman Osafo
%A Regina E. Abotsi
%J ISRN Pharmacology
%D 2013
%R 10.1155/2013/874263
%X Background. Various parts of Glyphaea brevis (Spreng) Monachino (Tiliaceae) find a use in traditional medicine in the treatment of pain and oedema among others. This study evaluates the anti-inflammatory, antiallergic, and antiarthritic effects of a 70% (v/v) aqueous ethanol extract of the stem bark of Glyphaea brevis in murine models. Materials and Methods. The effect of the aqueous ethanol extract of Glyphaea brevis extract (GBE) was assessed on the maximal and total oedema responses in the carrageenan-induced paw oedema in mice to evaluate the acute anti-inflammatory actions of the extract. Systemic anaphylaxis was induced with compound 48/80 and survival rates monitored for 1£¿h in mice with prior treatment with GBE to assess the anti-allergic action of the extract. The indirect antihistamine effect of GBE was evaluated on clonidine-induced catalepsy. Rat adjuvant-induced arthritis model was used to study GBE¡¯s antiarthritic action. Results. GBE significantly suppressed the mean maximal swelling and the total paw swellings over 6£¿h in the carrageenan-induced paw oedema when administered either prophylactically or therapeutically. GBE dose dependently increased the time for compound 48/80-induced mortality. Administered either prophylactically or therapeutically, GBE inhibited clonidine-induced catalepsy while it had no effect on haloperidol-induced catalepsy. GBE caused a significant dose-dependent suppression of Freund¡¯s adjuvant-induced arthritis. Conclusion. Glyphaea brevis inhibits the in vivo degranulation of mast cells and thereby suppress allergy. In addition it exhibits anti-inflammatory action and attenuates Freund¡¯s adjuvant-induced arthritis. The results of this work contribute to validate the traditional use of Glyphaea brevis in the management of inflammatory disorders. 1. Introduction Anaphylaxis is a rapid, life-threatening allergic reaction often triggered by food, drugs, insect venoms, latex, or allergen immunotherapy [1¨C5]. This acute allergic response is mediated by mast cells and basophils [6]. Mast cells express as one of their surface receptors the high affinity receptor for immunoglobulin E, IgE (Fc¦ÅRI) [7] and play a central role in the inflammatory and immediate-type allergic responses that occur when sensitised individuals contact allergen through body surfaces [8]. In the absence of an antigen, the Fc¦ÅRI binds to IgE. The major mechanism for the activation of these cells is the interaction of an antigen with the IgE-bound Fc¦ÅRI. An alternative pathway of activation of the mast cell is offered by the so-called peptidergic
%U http://www.hindawi.com/journals/isrn.pharmacology/2013/874263/