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Caffeic acid improves glucose utilization and maintains tissue ultrastructural morphology while modulating metabolic activities implicated in neurodegenerative disorders in isolated rat brains
Author(s) -
Salau Veronica F.,
Erukainure Ochuko L.,
Bharuth Vishal,
Islam Md. Shahidul
Publication year - 2021
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22610
Subject(s) - neuroprotection , biochemistry , biology , oxidative stress , nitric oxide , acetylcholinesterase , superoxide dismutase , ultrastructure , glucose uptake , glutathione , chemistry , catalase , endocrinology , microbiology and biotechnology , pharmacology , enzyme , anatomy , insulin
Impaired glucose utilization has been implicated in the pathophysiology of neurodegenerative diseases. The neuroprotective effect of caffeic acid (CA) was investigated in the isolated rat brain by determining its ability to promote glucose uptake, mitigate redox imbalance, modulate purinergic and cholinergic activities, elemental distribution, and maintain tissue morphology. Isolated rat brains were incubated for 2 hours with glucose, CA and glucose, and metformin and glucose. There was an increased glucose uptake, glutathione level, superoxide dismutase, and catalase activities in brain tissues incubated with CA compared to the controls. Incubation with CA also led to significantly decreased levels of malondialdehyde, nitric oxide, acetylcholinesterase, butyrylcholinesterase, and ATPase activities. Electron microscopy (scanning electron microscopy and transmission electron microscopy) analysis portrayed a maintenance of tissue ultrastructural morphology in 2CA‐incubated tissues as indicated by the intact synaptic vesicles, blood vessels, dendritic and neuronal network, mitochondria, and presynaptic membrane. CA also restored altered elemental levels in brain tissues. These results indicate the stimulatory potential of CA on brain glucose utilization with simultaneous neuroprotective activities.