Antidiabetic Investigations of Aqueous and Ethanol Extracts of Terminalia macroptera (Guill. & Perr.) Stem Bark in Streptozotocin-Induced Diabetic Wistar Rats
doi.org/10.26538/tjnpr/v5i6.25
Keywords:
Glucose, C-peptide, insulin gene, pancreatic duodenal homeobox-1, tumor necrosis factor-α, interleukin-1βAbstract
Diabetes mellitus always-increasing prevalence has prompted investigations into plants traditionally extolled for antidiabetic properties. One of such is Terminalia macroptera, a member of the Combretaceae family that grows in the Savannah. Consequently, this study evaluated the antidiabetic potentials of the stem bark aqueous (AE) and ethanol extracts (EE). Wistar rats were allotted into 2 controls (nondiabetic and diabetic) and 2 treatment (diabetic) groups (n = 5). All diabetic groups were induced intraperitoneally with streptozotocin (55 mg/kg body weight) from which respective treatment groups were orally administered AE and EE (200 mg/kg/day), while controls received water for 70 days. Thereafter, the concentrations of glucose, lipids, insulin, C-peptide, testosterone, and α-amylase activities were measured in serum. Liver homogenates were evaluated for glycogen and antioxidant status, while mRNA expressions of PDX-1, insulin-1, TNF-α, and Il-1 β were examined in β-cell. AE and EE, respectively, caused 55.66% and 78.95% reductions in elevated glucose when compared to control. However, only EE-treated rats had glucose and glycogen levels normalized besides increased insulin concentration (P < 0.05 vs diabetic control, DC). Both extracts significantly decreased lipid profiles but caused increase in antioxidant levels (P < 0.05 vs DC). In contrast to AE, EE slightly increased C-peptide and testosterone concentrations but significantly enhanced α-amylase activity. Up-regulated insulin gene expressions remained unabated, but those of PDX-1 and inflammatory factors were downregulated by both extracts (P < 0.05 vs DC). Terminalia macroptera stem bark was revealed to possess antidiabetic properties that were better expressed by EE through insulin stimulation.
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