B-234 Histopathological Changes in Some Organs of Diabetic Rats Administered Aqueous Extract of Beetroot or Glibenclamide

Abstract

Red beetroot (Beta vulgaris) is a traditional medicinal plant that contains bioactive compounds such as nitrates, phenolics, ascorbic acid, carotenoids, and betalains. Although raw beetroot consumption has been associated with potential benefits in diabetes, its safety and histopathological effects require further investigation. This study evaluated the effects of aqueous beetroot extract on histopathological changes in the heart, pancreas, liver, and kidney of normal and streptozotocin-induced diabetic rats, compared with glibenclamide treatment. Twenty-five Sprague Dawley rats (mean body weight 187.16 ± 7.20 g) were randomized into five groups (n=5/group): healthy control (deionized water), healthy + aqueous extract, diabetic control (deionized water), diabetic + aqueous extract, and diabetic + glibenclamide. Diabetes was induced by a single intraperitoneal injection of streptozotocin (60 mg/kg in 0.05 M citrate buffer, pH 4.5). For 30 days, treated groups received aqueous beetroot extract (500 mg/kg/day) or glibenclamide (5 mg/kg/day). After euthanasia by decapitation, blood was collected for glucose measurement, and the heart, and kidney were harvested for histopathological evaluation following fixation in 10% buffered formalin Diabetic rats treated with aqueous extract or glibenclamide demonstrated a significant reduction in blood glucose compared with diabetic controls (p<0.05). In the heart, diabetic controls exhibited severe vascular stenosis, myocardial degeneration, vascular ulceration, and inflammatory infiltrates. These changes were markedly attenuated in extract- and glibenclamide-treated diabetic rats, which showed largely preserved vascular architecture with mild congestion. Pancreatic sections from diabetic controls showed vascular stenosis, hypoplasia, lymphoid aggregates, ulceration, and reduced islets of Langerhans. Treatment with the aqueous extract restored islet architecture and vasculature, comparable to that achieved with glibenclamide. In the liver, diabetic controls demonstrated portal vascular congestion, and periportal inflammatory infiltrates. Diabetic groups treated with the extract or glibenclamide showed preserved hepatocyte morphology with only mild vascular congestion. Renal histology in diabetic controls revealed glomerular abnormalities, including shrunken vascular meshwork (Kimmelstiel–Wilson–like nodules), vascular hypertrophy, stenosis, and focal tubular necrosis. Extract-treated diabetic rats showed improved vascular architecture with only focal glomerular damage, while glibenclamide-treated rats demonstrated persistent glomerular changes relative to diabetic controls. Aqueous beetroot extract significantly reduced hyperglycemia and attenuated diabetes-associated histopathological damage in the heart, and kidney. Restoration of vascular architecture and pancreatic islet structure suggests a potential protective role against diabetic complications. These findings support further investigation of beetroot extract as a complementary therapeutic strategy in diabetes management.