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Background: Renal failure is among the main complications of diabetes disorders and free radical from hyperglycemia is the major cause of this nephrotic complication. This study investigated the therapeutic effects of Bridelia ferruginea Benth on nephrotic damage in streptozotocin (STZ) induced diabetic rats. Diabetes mellitus was induced by injection of 50 mg/kg b. w. of STZ (intraperitoneal) in rats fasted overnight. Effect on nephropathy was assessed using biochemical, histological indices and gene expression of kidney tissue. Results: The total flavonoids and phenolic content of petroleum ether fraction of B. ferruginea (PEFBF) was observed to be higher compared to diethyl ether fraction of B. ferruginea (DEFBF). The 1,1-diphenyl-2-picryl-hydrazyl scavenging activity of the fractions were significantly (P < 0.05) reduced across the concentrations compared to the standard (gallic acid). The STZinduced diabetic animals treated with 100 and 200 mg/kg b.w. of PEFBF and DEFBF showed significant (P < 0.05) reduction in blood glucose level on days 7, 11 and 14 compared to untreated diabetic rats. STZ-induced diabetic rats significantly (P < 0.05) exhibited increase plasma urea, creatinine, protein and albumin level while treatment with both fractions of B. ferruginea reduced the level of these parameters in treated diabetic rats. B. ferruginea also caused down-regulation of neutrophil gelatinase-associated lipocalin, kidney injury molecule-1 and cystatin c genes. Conclusion: These results revealed that, the plant has hypoglycemic activity therefore provides a pharmacological basis for its folkloric use in the management of hyperglycemia and its associated renal dysfunction.

Background: The anti-hyperglycemic potential of methanol stem bark extract of Anacardium occidentale (MSBEAO) was investigated using an alloxan-induced diabetic rat model. Alloxan administration induces the generation of free radicals which can affect antioxidant status resulting in the disruption of the β-cells of the pancreas. Therefore, this study examines the antioxidant potential of the plant extract and the ameliorating effect on the pancreas of alloxan-induced diabetic rats. Methods: Diabetes was induced by intraperitoneal injection of 150 mg/kg body weight of alloxan monohydrate. MSBEAO, at a concentration of 100 or 200 mg/kg b.w. was orally administered to alloxan-induced diabetic rats and normal rats. The hypoglycemic effect, oral glucose tolerance test, and biochemical assay of alloxan-induced diabetic rats were assayed using standard procedures. Results: Preliminary phytochemical screening of the extract revealed the presence of alkaloids, tannins, saponins, terpenoids, carbohydrates, and phenols at moderate concentrations. The lethality dose (LD50) of the plant extract was found to be equal to or less than 5000 mg/kg b.w. The hypoglycemic effect of the extract on the non-diabetic rats revealed a significant (p<0.05) decrease in the blood glucose concentration of animals administered with 1 g/kg b.w. of the extract, compared to normal control rats administered with normal saline. In the oral glucose tolerance test, the methanol extract exerted the highest response, similar to glibenclamide after 15 and 30 minutes of administration, compared to the control rats. The methanol extract yielded the highest blood glucose lowering effects after 9 days of treatment (p<0.05), compared to diabetic rats administered with normal saline and 0.3 mg/kg b.w. of glibenclamide. Administration of the extract at 200 mg/kg b.w. showed improved pancreas architecture and regeneration of the β-cells, compared with the pancreas of animals in the other groups. Conclusion: The results of this study suggest that MSBEAO is a potentially effective agent for the management of diabetes which might result from the antioxidant-generating capacity of the stem bark.

The purpose of this study was to investigate the synergistic effects of calcium ion-protein energy malnutrition (Ca2+-PEM) and methanolic extract of Plumbago zeylanica (Pz) root on mitochondria permeability transition pore (MPTP). Twenty-four male Wistar rats were studied. The Wistar rats were divided into two groups (experimental and control) of 12 each. The experimental rats were fed with protein-deficient diet, and the control rats were fed with normal rat chow and water ad libitum for 42 days. To monitor MPTP induction and inhibition in both experimental and control Wistar rats, 3 mM Ca2+, 1 mM Mg2+, 120, 160, and 200 μg/ml of Pz extract were used. The rats were sacrificed, and mitochondria were isolated from the livers to monitor MPTP. Our study showed that Ca2+ and Mg2+ induced and inhibited MPTP, respectively. However, PEM drastically increased Ca2+ and Mg2+ MPTP induction and inhibition, respectively, when compared to control. At varying dose and timing, Pz extracts steadily induce MPTP in both experimental and control Wistar rats. Taken together, the results suggest that Ca2+-PEM increased the MPTP induction, while PEM decreased the MPTP induction of Pz extract in dose- and time-dependent pattern when compared to the control that plausibly suggests that PEM may increase Ca2+ induction of MPTP as well mitigate therapeutic effects of Pz extract in diseases related to mitochondria targeting.