Preclinical antidiabetic and antioxidant effects of Erythrophleum africanum (benth.) harms in streptozotocin-induced diabetic nephropathy
Author:
Ojo Oluwafemi A.12ORCID, Ajeigbe David12, Ogunlakin Akingbolabo D.12, Odesanmi Olalekan E.3, Ayomipo Mojisola12, Berana Godwin12, Ayeni Peluola12, Ajayi-Odoko Omolola A.4, Ayokunle Damilare I.5, Ojo Adebola B.3, Ajiboye Basiru O.6, Ojo Omolara O.3, Dahunsi Samuel O.4
Affiliation:
1. 70671 Good Health and Wellbeing Research Clusters (SDG 03), Bowen University , Iwo , Nigeria 2. Biochemistry Programme , 70671 Phytomedicine, Molecular Toxicology, and Computational Biochemistry Research Laboratory (PMTCB-RL), Bowen University , Iwo , Nigeria 3. Department of Biochemistry , Ekiti State University , Ado-Ekiti , Nigeria 4. Microbiology Programme , 70671 Bowen University , Iwo , Nigeria 5. Pure and Applied Biology Programme , 70671 Bowen University , Iwo , Nigeria 6. Department of Biochemistry , Federal University Oye Ekiti , Oye Ekiti , Nigeria
Abstract
Abstract
Objectives
This study investigated the antidiabetic effects of the methanolic extract of E. africanum (MEEA) stem bark on streptozotocin (STZ)-induced diabetic nephropathy (DN) in Wistar rats.
Methods
The in vitro enzyme (α-amylase) inhibitory activity of MEEA was measured using a standard procedure. Diabetic rats with fasting blood glucose above 250 mg/dL were considered diabetic and were divided into the following groups: control (distilled water-treated), diabetic-control, diabetic metformin (100 mg/kg), diabetes + MEEA (150 mg/kg), and diabetes + MEEA (300 mg/kg) via oral gavage once daily for 14 days. At the end of the experimental period, kidney tissues were collected for biochemical and histological analyses. Kidney apoptosis and marker gene expression were measured by real-time quantitative PCR.
Results
MEEA exhibited α-amylase inhibitory effects. MEEA significantly (p<0.05) reduced the STZ-induced increases in blood glucose, serum urea, serum creatinine, uric acid, alanine aminotransferase, alkaline phosphatase, and malondialdehyde and increased the STZ-induced decreases in superoxide dismutase, catalase, and reduced glutathione. In addition, MEEA protects against DN by significantly downregulating the mRNA expression of cyclic adenosine monophosphate (cAMP), protein kinase A (PKA), cAMP-response binding protein (CREB), and cFOS and upregulating B-cell lymphoma 2 (Bcl-2), suggesting that the nephroprotective ability of MEEA is due to the modulation of the cAMP/PKA/CREB/cFOS signaling pathway. Furthermore, MEEA treatment protected against histopathological alterations observed in diabetic rats.
Conclusions
The data from this study suggest that MEEA modulates glucose homeostasis and inhibits redox imbalance in DN rats.
Publisher
Walter de Gruyter GmbH
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