Anti-denaturation, Antioxidant, and Antidiabetic Investigations of Terminalia macroptera (Guill. & Perr.) Stem Bark Alkaloids: in vitro and in vivo Studies

Ambrose Akpovona, Iyere Onoagbe, Usunomena Usunobun, Destiny Akoma and Precious Uzomah

Background and Objective: Terminalia macroptera (Guill. & Perr.) is a West African plant used against several diseases, including diabetes mellitus. However, its glucose regulatory mechanism remains unclear. Therefore, this study examined the effects of Terminalia macroptera stem bark alkaloids (TMSBA) on protein denaturation, free radicals, and carbohydrate hydrolases, with a further investigation of the alkaloids’ action on the biochemical indices of streptozotocin-induced diabetic rats. Materials and Methods: The in vitro properties of TMSBA were investigated by spectrophotometry, while in vivo studies compared the 10-week treatment outcomes of TMSBA (100 mg/kg/day) and glibenclamide (GLIB) (10 mg/kg/day) in the rats. Analyses entailed the evaluation of blood glucose, serum lipids, insulin, C-peptide, testosterone, pancreatic amylase activity, liver glycogen, and antioxidants. In addition, the β-cell mRNA of pancreatic-duodenal homeobox 1, insulin, and inflammatory factor genes were extracted and compared. Data, expressed in mean ± SEM (n = 5), were subjected to a one-way analysis of variance (ANOVA) and followed by the Tukey’s post hoc test. Results: The findings showed that TMSBA mimicked the concentration-dependent manner of reference compounds in albumin-binding, antioxidant, and hydrolase inhibition but with less strength. More so, it scavenged hydroxyl radicals at maximum and minimum concentrations non-significantly different from thiourea and neutralized peroxyl radicals at a rate similar to vitamin C (TMSBA IC₅₀ = 510.583±65.684 vs ascorbic acid IC₅₀ = 565.661±68.011 μg/mL). Conclusion: TMSBA demonstrated a non-insulin-mediated normalization of the glucose and lipid benchmarks better than GLIB (p < 0.05). Also, it stimulated more glycogen, restored antioxidants, and downregulated the gene expressions of pancreatic-duodenal homeobox 1, insulin, and stress factors compared to GLIB.

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