Antinociceptive Activity ofMelicope ptelefoliaEthanolic Extract in Experimental Animals

Abstract

Melicope ptelefolia is a medicinal herb commonly used in Malaysia to treat fever, pain, wounds, and itches. The present study was conducted to evaluate the antinociceptive activity of the Melicope ptelefolia ethanolic extract (MPEE) using animal models of nociception. The antinociceptive activity of the extract was assessed using acetic acid-induced abdominal writhing, hot-plate, and formalin-induced paw licking tests. Oral administration of MPEE produced significant dose-dependent antinociceptive effects when tested in mice and rats using acetic acid-induced abdominal constriction test and on the second phase of the formalin-induced paw licking test, respectively. It was also demonstrated that MPEE had no effect on the response latency time to the heat stimulus in the thermal model of the hot-plate test. In addition, the antinociception produced by MPEE was not blocked by naloxone. Furthermore, oral administration of MPEE did not produce any effect in motor performance of the rota-rod test and in acute toxicity study no abnormal behaviors as well as mortality were observed up to a dose level of the extract of 5 g/kg. These results indicated that MPEE at all doses investigated which did not produce any sedative and toxic effects exerted pronounce antinociceptive activity that acts peripherally in experimental animals.

Antinociceptive and Anti-inflammatory Activities of Methanol Extract of Ormosia coccinea (Aubl.) Jacks in vivo

“…The acetic acid-induced abdominal writhing test is a peritoneo visceral inflammatory pain model [16] widely used to evaluate peripheral antinociceptive activity [19,20]. Because this model is highly sensitive and also has the ability to detect antinociceptive effects of compounds at dose levels that may appear inactive in other models [20,21].…”

“…Because this model is highly sensitive and also has the ability to detect antinociceptive effects of compounds at dose levels that may appear inactive in other models [20,21]. The intraperitoneal administration of agents that irritate serous membranes provokes a stereotyped behaviour in the mice which is characterized by abdominal contractions, movements of the body as a whole and twisting of the dorso-abdominal muscles [22] and a reduction in motor activity and motor incoordination [23].…”

“…The intraperitoneal administration of agents that irritate serous membranes provokes a stereotyped behaviour in the mice which is characterized by abdominal contractions, movements of the body as a whole and twisting of the dorso-abdominal muscles [22] and a reduction in motor activity and motor incoordination [23]. It has been suggested that acetic acid injection into peritoneal cavity leads to increased levels of cyclooxygenases (COX) and lipoxygenase [24] and indirectly leads to the release of endogenous nociceptive mediators such as PGE 2 and PGF 2α [5,20,[25][26][27][28][29][30], serotonin [22,25,26,29,30], histamine [22,26,30,31], bradykinin [21,22,24], substance P [24,25], cytokines (TNF-α, IL-1β, IL-8) [21,24,25,29] and lipoxygenase products [20], which eventually excites the primary afferent nociceptors [25] that contribute to the development of inflammatory pain [22]. The data presented in Fig.…”

“…It is a widely used model, particularly for the screening of novel compounds, since it encompasses inflammatory, neurogenic, and central mechanisms of nociception [33]. Intraplantar injection of formalin has been reported to produce a distinct biphasic nociceptive response [12,21], termed first and second phases [20]. The first phase, commonly denominated early or neurogenic phase (from 0 to 5 min after injection formalin) results from a direct stimulation of nociceptors (predominantly C-fibres) [22,23,27,28,31,32,34].…”

“…Substance P, glutamate and bradykinin are thought to participate in this phase, which is believed to be non-inflammatory pain [28]. The second phase, commonly denominated late or inflammatory phase (from 15 a 30 min) [29] is associated with the release of local endogenous mediators (histamine, serotonin, prostaglandins and bradykinin) responsible for sensitization of primary and spinal sensory neurons and subsequent activation of the nociceptor [20,25,34]. It is well established that both phases of the formalin test can be inhibited by centrally acting drug, such as narcotics, whereas peripherally acting drugs, such as acetylsalicylic acid, only inhibit the second phase [21,22,29,30].…”