ABSTRACT
Background:A good number of medicinal and dietary plants are used for diabetes treatment in Burkina Faso. Aim of the Study:The present study aimed to investigate the antidiabetic activity of Guiera senegalensisgalls extracts and its potential mechanisms in streptozotocin-induced diabetic rats. Methodology:The methanol extract was administered by gavage to healthy Wistar rats for the determination of toxicity, to normal and diabetic Wistar rats forthe determination of glucose reduction level, lipid profile, insulin level and glycaemic parameters in serum. The histology and immunohistochemistry of thepancreas were also determined.Results:The acute toxicity results showed that the medium lethal dose (LD50) of the methanol galls extract of Guiera senegalensisis greater than 2000 mg/kg body weight in rats. Guiera senegalensismethanolic extract (250 mg/kg) and the tolbutamide (100 mg/kg) recorded a significantly (p < 0.05)lower level of triglyceride compared to the diabetic group. The methanol extract (250 and 500 mg/kg pc) significantly (p < 0.05)decreased the blood glucose level and increased the serum insulin level in diabetic rats. Interestingly, improved ß-cell function and antioxidant status were also observed in G. senegalensis-treated diabetic rats when compared to tolbutamide-treated diabetic rats.Conclusion:These data showed direct evidence that G. senegalensishas antidiabetic activity by decreasing blood glucose level, improving insulin secretion and β-cell functions and modulating antioxidant status
ABSTRACT
Objective: To investigate the possible mechanism and the compound(s) responsible for the antiplatelet and acetylcholinesterase (AChE) inhibitory effects of Areca catechu crude extract (Ac.Cr). Methods: Aqueous-methanol (70%) was used for extraction of plant material (betel nut). Antiplatelet activity was measured in human platelet-rich plasma by using a Lumi-aggregometer while anti-AChE activity was measured spectrophotometrically in vitro. In an attempt to find the responsible compound(s) in betel nut for antiplatelet and anti-AChE activities, different commercially available betel nut compounds were tested. Results: Ac.Cr inhibited platelet aggregation induced by arachidonic acid (AA), adenosine diphosphate (ADP), platelet-activating factor (PAF), epinephrine and Ca(2+)-ionophore. Ac.Cr was the most potent in inhibiting ADP- and Ca(2+)-ionophore-induced aggregation. In the AChE assay, Ac.Cr showed significant AChE inhibitory activity with almost complete inhibition of the enzyme. Out of the tested compounds, none of the compounds in betel nut showed any antiplatelet effect except for catechin that was the most potent against epinephrine-induced aggregation. Catechin was significantly less potent than Ac.Cr, indicating a presence of additional compound(s) with antiplatelet activity. For the AChE inhibitory effect, only tannic acid, gallic acid, diosgenin and isoguvacine were found to be active, whereby tannic acid was more potent than Ac.Cr. Conclusion: This study shows the possible antiplatelet and AChE inhibitory potential of betel nut while further studies are needed to confirm and identify more compounds in betel nut for these actions.