Co-administration of Spondias mombin and Metformin mitigates Streptozotocin-induced hepatorenal injury

•Streptozotocin resulted in hepatorenal histopathology.•Co-administration of Spondias mombin with metformin reversed these alterations.•Spondias mombin and metformin treatments demonstrated anti-hyperglycaemic activity.•Spondias mombin showed anti-oxidative potentials.•Spondias mombin showed anti-apoptotic potentials in the liver but not the kidney. As a result of its many therapeutic properties, including its potent anti-hyperglycemic effect, the Spondias mombin plant is quickly gaining popularity as a local therapeutic agent for the treatment of many ailments. This work aimed at investigating the effects of co-administration of Spondias mombin and metformin in STZ-induced hyperglycemia and hepatorenal injury in the Wistar rat model, specifically focusing on the morphological, biochemical, and immunohistochemical alterations in the liver and kidney. Hundred healthy adult male Wistar rats weighing (80-150g) and assigned into 10 groups (A-J) (n= 10 each). The normal control group A received a single dose of citrate buffer (1mL/kg, p.o) while groups B, C, D, E, F, and I were induced with hyperglycemia by administering a single dose of Streptozotocin (60 mg/kg, i.p). Group B was left untreated while others were treated with Spondias mombin (600 mg/kg p.o), (400 mg/kg p.o), (200 mg/kg p.o), metformin (12.5 mg/kg p.o), and Spondias mombin + metformin (12.5 mg/kg) respectively. Groups G and H were administered Spondias mombin only (400 mg/kg) and metformin (12.5 mg/kg) respectively; and group J was not induced but administered both Spondias mombin only (400 mg/kg) and metformin (12.5 mg/kg). Administration in all groups lasted for 28 days. Rats were sacrificed and the liver and renal tissues were excised for histopathological examination using the H&E stain, while the Periodic acid Schiff reagent, and Masson Trichome stains were employed for connective tissue assessments. Oxidative stress parameters (CAT, SOD, GSH, and MDA) were evaluated. The assessment of liver enzymes (ALT, AST, and ALP) and renal markers (Urea, and Creatinine) were also carried out. Kidney and liver Bcl-2 expressions were assessed immunohistochemically. The data obtained were analyzed by ANOVA and Duncan Multiple Range post hoc test and presented as mean ± SEM at p