Therapeutic effects of balanitoside in streptozotocin-induced diabetic rats

Abstract

Objectives The objective of this study was to evaluate the therapeutic effects of balanitoside in diabetic rats. Methods Twenty-five rats were divided into five groups. Rats in groups 2 to 5 were treated with streptozotocin to induce hyperglycemia. In addition, rats in groups 1 and 2 received 1 mL of distilled water, whereas those in groups 3, 4, and 5 received 10 and 20 mg/kg balanitoside and 6 U/kg insulin, respectively, for 14 days. All rats were sacrificed on day 15, blood samples were collected, and serum levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were measured. The liver was processed for examination under a light microscope. Results The results showed a significant decrease in liver protein concentrations in diabetic control rats, compared to those in the normal control rats and rats treated with 10 mg/kg balanitoside ( p < 0.05). There was no significant difference in ALP levels among all groups. However, a significant increase in ALT and AST levels was observed in the diabetic control rats, compared to those in the normal control rats ( p < 0.05). Photomicrographs of the liver of the diabetic control rats showed fat and glycogen droplets, vacuolated nuclei, and loss of cellular boundaries, whereas those of the rats treated with balanitoside or insulin showed a small amount of microvesicular fat droplets and slight infiltration of lymphocytes. Conclusion The findings of this study suggest the therapeutic effects of balanitoside in the liver of diabetic rats.

Melatonin downregulates the increased hepatic alpha-fetoprotein expression and restores pancreatic beta cells in a streptozotocin-induced diabetic rat model: a clinical, biochemical, immunohistochemical, and descriptive histopathological study

“…Similarly, in a previous study, livers from DM rats revealed disturbed hepatic architecture, pericentral sinusoidal dilatation, apoptosis, and lipid droplet accumulation in hepatocytes, in addition to signs of inflammation ( 44 ). Additionally, the degeneration of liver cells and the congestion of blood vessels with periportal fibrosis were reported in previous studies ( 48 , 54 , 55 ). Histopathological changes due to STZ administration observed in our study were similarly observed in previous studies ( 1 , 56 ).…”

Fustin ameliorates hyperglycemia in streptozotocin induced type-2 diabetes via modulating glutathione/Superoxide dismutase/Catalase expressions, suppress lipid peroxidation and regulates histopathological changes

“…The findings revealed elevated blood glucose levels after diabetes induction and a rise in the levels of liver enzymes (ALT and AST) in diabetic rat’s serum. The substantial rise in ALT and AST levels in diabetic control rats indicated that diabetes mellitus could cause hepatic damage, possibly due to the increase in protein concentrations associated with glucogenesis and urea production found in the diabetic state ( Makena et al, 2018 ). When compared to rats given 50 mg/kg fustin, rats given 100 mg/kg fustin reported a slight rise in ALT and AST levels, suggesting that fustin at 100 mg/kg could have therapeutic effects in the hepatocytes by lowering ALT and AST levels.…”

Inflammatory atherosclerotic plaque identification by SPECT/CT imaging of LFA-1 using [111In] In-DANBIRT in a novel dyslipidemic rat model

“…Increase in ALP and ALT has been most closely associated with liver damage in metabolic disease evolution [12,13]. Increase in liver enzymes has shown to be directly correlated to the development of diabetes phenotype in rats [14,15]. Similar observations have been made in diabetic patients [16].…”