Therapeutic Potential of Dillenia indica L. in Attenuating Hyperglycemia-Induced Oxidative Stress and Apoptosis in Alloxan-Administered Diabetic Mice

Front Biosci (Landmark Ed). 2023 May 26;28(5):105. doi: 10.31083/j.fbl2805105.

Abstract

Background: Hyperglycemia-induced oxidative stress accelerates the process of apoptosis in tissues. Dilleniaindica (DI) is a medicinal plant, and its fruit contains many therapeutic properties. The therapeutic activity of the Methanolic Fruit Extract (MFE) of DI in attenuating oxidative stress and apoptosis in the liver and kidney tissues of alloxan-induced diabetic mice was analyzed in the present study.

Methods: High-Performance Thin Layer Chromatography (HPTLC) profiling of MFE was conducted. GLUT4 protein expression analysis and lipid peroxidation assays were conducted to check for MFE effect by administering in diabetic mice. An ultrastructural study was conducted for both the tissues. In apoptotic studies, the TUNEL assay and apoptotic protein expression analysis was conducted.

Results: High-Performance Thin Layer Chromatography (HPTLC) profiling of MFE showed the presence of two crucial antioxidants, ascorbic acid, and naringenin. In GLUT-4 protein expression analysis, MFE suppresses hyperglycemia by upregulating GLUT4 protein expression. Lipid peroxidation assay showed a decrease in malondialdehyde (MDA) upon MFE administration in diabetic mice. An ultrastructural study was conducted, and MFE was found to restore cellular alterations in diabetic tissues. In apoptotic studies, the TUNEL assay shows that MFE treatment showed fewer apoptotic cells than the diabetic group. The study also observed decreased caspase 3 protein expression and increased Bcl-2 protein expression.

Conclusions: Therefore, it is inferred from the study that MFE can exert a protective effect by suppressing hyperglycemia and modulating oxidative stress and apoptosis in alloxan-administered diabetic mice.

Keywords: Dillenia indica extract; HPTLC; alloxan; apoptosis; hyperglycemia; oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alloxan / pharmacology
  • Alloxan / therapeutic use
  • Animals
  • Antioxidants / metabolism
  • Apoptosis
  • Diabetes Mellitus, Experimental* / metabolism
  • Dilleniaceae* / metabolism
  • Glucose Transporter Type 4 / genetics
  • Glucose Transporter Type 4 / metabolism
  • Hyperglycemia* / drug therapy
  • Hyperglycemia* / metabolism
  • Mice
  • Oxidative Stress

Substances

  • Alloxan
  • Glucose Transporter Type 4
  • Antioxidants