Evaluation of the biological efficiency of Terminalia chebula fruit extract against neurochemical changes induced in brain of diabetic rats: an epigenetic study.
Marwa E A El-ShamarkaWael Mahmoud Kamel AboulthanaNagwa Ibrahim OmarMarwa M MahfouzPublished in: Inflammopharmacology (2024)
Diabetes mellitus (DM) is a chronic and progressive metabolic disorder that can stimulate neuroinflammation and increase oxidative stress in the brain. Therefore, the present study was aimed to assess the efficacy of ethanolic Terminalia chebula extract against the neurochemical and histopathological changes induced in the brains of diabetic rats. The study clarified the reduction in oxidative stress induced in the brains of diabetic rats by the significant (P ≤ 0.05) increase in levels of the antioxidants with decreasing the peroxidation products via ethanolic T. chebula extract at both doses (400 and 600 mg/kg). Moreover, T. chebula extract improved the brain integrity by lowering levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), β-amyloid (Aβ) content, monocyte chemoattractant protein-1 (MCP-1) and acetylcholine esterase (ACHE) significantly (P ≤ 0.05) in a dose dependent manner compared to brain of diabetic rats. Severe nuclear pyknosis and degeneration were noticed in neurons of the cerebral cortex, hippocampus and striatum in brains of diabetic rats. The severity of these alterations decreased with T. chebula extract at a dose of 600 mg/kg compared to the other treated groups. The different electrophoretic protein and isoenzyme assays revealed that the lowest similarity index (SI%) values exist in the brains of diabetic rats compared to the control group. The quantity of the most native proteins and isoenzyme types increased significantly (P ≤ 0.05) in the brains of diabetic rats, and these electrophoretic variations were completely diminished by T. chebula extract. The study concluded that T. chebula extract ameliorated the biochemical, histopathological and electrophoretic abnormalities induced in the brains of diabetic rats when administered at a dose of 600 mg/kg.
Keyphrases
- diabetic rats
- oxidative stress
- ischemia reperfusion injury
- induced apoptosis
- dna damage
- white matter
- rheumatoid arthritis
- dendritic cells
- cerebral ischemia
- type diabetes
- traumatic brain injury
- immune response
- single cell
- small molecule
- protein protein
- spinal cord injury
- binding protein
- anti inflammatory
- blood brain barrier
- amino acid
- lps induced