Vernonia Amygdalina Del. stimulated glucose uptake in brain tissues enhances antioxidative activities; and modulates functional chemistry and dysregulated metabolic pathways

Abstract

Brain glucose uptake is usually reduced in type 2 diabetes owing to downregulation of brain glucose transporters. The ability of Vernonia amygdalina to stimulate glucose uptake as well as ameliorate glucose-induced oxidative stress and proinflammation were investigated in rat brain. Hot infusion of V. amygdalina leaves was incubated with rat brain tissues for 2 h in the presence of glucose. Another incubation with glucose only, served as negative control while metformin served as positive control. Incubation of brain tissues with V. amygdalina led to significant (p < 0.05) increase in glucose uptake, reduced glutathione, nitric oxide and non-thiol proteins levels, superoxide dismutase, catalase and ATPase activities, while concomitantly decrease in myeloperoxidase activity and malondialdehyde level compared to the negative control. Incubation with glucose only, led to the development of nitrate, amide II and amide I functional groups which were removed on incubation with the infusion. LC-MS analysis revealed depletion of oxidative stress-induced 2-keto-glutaramic acid and cysteinyl-tyrosine metabolites in brain tissues, with concomitant generation of S-formylglutathione and adenosine tetraphosphate by the infusion. Pathway analysis of the metabolites revealed an activation of pyruvate metabolism pathway in the negative control, with the infusion reducing the intensity fold. LC-MS analysis of the infusion revealed the presence of l-serine, l-cysteine, l-proline, nicotinic acid, cumidine, salicylic acid, isoquinoline, 3-methyl-, and γ-octalactone. Except for l-serine, l-cysteine and l-proline, the other compounds were predicted to be permeable across the blood brain barrier. These results indicate the brain glucose uptake stimulatory and neuroprotective effect of V. amygdalina.

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“…With the effect of Vernonia amygdalina that contains the structure of terpenoids on the cells of the rat brain tissue, it has been shown that in conditions of HG uptake in these cells, the amount of ROS increased, the amount of glutathione decreased, and thus the amount of NO also changed 83. Therefore, increased antioxidant availability may be helpful in preventing or slowing the progress of various oxidative stress-related diseases 84…”

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“…72 Also, it was capable of stimulating glucose uptake in rat brain as well as showing neuroprotective effects. 73…”

Catechol protects against iron-mediated oxidative brain injury by restoring antioxidative metabolic pathways; and modulation of purinergic and cholinergic enzymes activities

“…The nitric oxide (NO) level of the experimental tissue samples was determined using the Griess method as previously described. [1,28] Briefly, 100 μl of brain supernatant or distilled water (serving as the blank) was added to equal volume of Griess reagent and incubated for 30 min at 25°C in the dark. Absorbance was then read at 548 nm.…”

“…Oxidative stress is amongst the major drivers of complications associated with the pathogenesis of neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. [1,2] This has been attributed to the dependency of the brain on glucose and oxygen (O 2 ), coupled with its high polyunsaturated fatty acids, low endogenous antioxidant system and redox-active metal load. [3,4] Of these redox-active metals, iron has been reported to be one of the most potent prooxidants.…”