Antiemetic Activity Of A. Julibrissin Flowers Case Study

This paper is the first to indicate antiemetic activity of the methanolic extract compositions of A. julibrissin flowers and its protective effect on mitochondria disruption induced by retching in brain of the young chickens.
Nausea and vomiting are the symptoms of drug side effects, different disease and defenses responsive against poisoning. Recently, extensive researches have led to use of medicinal plants as a safe and reliable source of drugs with low or lack of toxicity and side effects [22, 23]. A. julibrissin is one of the medicinal plants that generally is used in numerous disease because of its effectiveness. This plant contains of different compounds such as flavonoids julibrosids, terpenes, phenolic compounds, alkaloids and lignans
Flavonoids, glucosides, lignans, saponins and terpenes are the class of compounds which have been identified as antiemetic activities. The proposed multiple mechanisms of action for these natural products are probably due to inhibition of dopaminergic stimulation of the visceral afferent innervations, antioxidant action, 5-HT3 /5-HT4 receptors antagonism, δ (enkephalinergic)-receptor inhibition, tachykinin NK1 receptors antagonism, cannabinoid CB1 receptor activation [6]. Therefore, behalf of the presence of these compounds in the tested extract, it could be implied that they may be involved in the antiemetic activity of the extract. Further studies are required concerning the active compounds and the mechanism of action responsible for antiemetic activity of the extract. It may be that extract has a similar effect to metoclopramide by stimulation of the motility of the upper gastrointestinal tract and accelerates the gastric emptying rate. According to the mechanism of retching, emesis can produce by the stimulation of the dopaminergic neurones at the CTZ. On the other hand, release of the 5-hydroxytryptamine (5-HT) from the enterochromaffin cells can occur
They act either by reducing the energy of the free radicals or by giving up some of their electrons to them, thereby causing to become stable. In addition, they may also interrupt the oxidizing chain reaction to minimize the damage induced by free radicals. Therefore, increase of mitochondrial function in the treated groups in our study (figure 3, 4) can be due to the present of high content of the antioxidant compounds in the tested extract. Further studies are necessary regarding the mechanism of action the active extract compounds responsible for the mitochondrial damage