Abstract

The process of protein glycation is one of the major causes of diabetic nephropathy, which severely destroys the glomeruli within the kidney and is the leading cause of death in diabetic patients. The goal of this work was to assess the antiglycation and antioxidant capacity of 11-Keto--Boswellic Acid (KBA) and 5-Chloro-8-Hydroxyquinoline (CHQ) in vitro, as well as to investigate kidney damage in streptozotocininduced diabetic mice and investigate their probable mechanisms of action. CHQ showed a significant antiglycation effect in the antiglycation assay, with an IC50 value of <50μM, whereas KBA demonstrated good activity with an IC50=146.662.5μM when compared to rutin (IC50=98.01 2.03M) employed as a standard antiglycation agent. In 10–12-week-old CD1 mice, diabetes was induced by injecting 180mg/ kg of Streptozotocin (STZ) intraperitoneally. The normal mice group, the diabetic mice group, the KBA treated mice group, and the CHQ treated mice group were separated into four groups two weeks after STZ injection. The KBA and CHQ-treated mice received a 25mg/kg intraperitoneal dosage of KBA and CHQ, respectively. The blood glucose level (237.6 23.4mg/dl) measured after six weeks of STZ injection in the KBA treated mice group was significantly lower than the blood glucose level (415.8 25.2mg/dl) measured after two weeks. Histopathological changes in kidney structure confirmed that renal damage was reduced by reducing the enlargement of the mesangial matrix of the glomerulus in the nephron and significantly restoring Bowman’s gap in KBA and CHQ treated mice. The hypoglycemic action of KBA and antiglycation activity of CHQ can be linked with reduced kidney damage.

Keywords:Diabetic nephropathy; 11-Keto--boswellic acid; 5-Chloro-8-hydroxyquinoline; Streptozotocin-induced diabetic mice; Histopathology; Antiglycation; Antioxidant

Abbreviations:KBA: 11-Keto--Boswellic Acid; CHQ: 5-Chloro-8-Hydroxyquinoline; ROS: Reactive Oxygen Species; BSA: Bovine Serum Albumin; GFR: Glomerular Filtration Rate