Abstract
Objective The present study was designed to evaluate the neuroprotective effects of D-(-)-quinic acid on aluminum chloride- (AlCl3-) induced neurobehavioral and biochemical changes in rats. This study showed the behavioral and biochemical effects of D-(-)-quinic acid on rats with particular emphasis on the hippocampus and frontal cortex which are associated with memory. Materials and Methods Chronic administration of aluminum chloride at a dose of 175 mg/kg, p.o. for a period of 25 days markedly increased the level of acetylcholinesterase (AChE) activity and reduced the levels of antioxidant enzymes in the brain. Two doses of D-(-)-quinic acid (200 mg/kg and 400 mg/kg) were selected based on previous safety/toxicity studies and administered orally from the 26th day to the 36th day of the trial. Behavioral parameters were assessed using the Morris water maze test and an actophotometer in rats. Biochemical parameter content and histology of brain tissue were assessed on the final day of the experiment. Results D-(-)-Quinic acid (200 mg/kg and 400 mg/kg) orally administered alongside AlCl3 rescued AChE activity and the behavioral impairments caused by aluminum. There was significant inhibition of MAO-B in D-(-)-quinic acid-treated rats. Histopathological studies in the hippocampus and cortex of the rat brain also supported that D-(-)-quinic acid markedly reduced the toxicity of AlCl3 and preserved the normal histoarchitecture pattern of the hippocampus and cortex. These results indicate that D-(-)-quinic acid can reverse memory loss caused by aluminum intoxication by attenuating AChE activity and rescuing the deleterious effect of AlCl3.
Highlights
Neurodegenerative diseases such as Alzheimer’s disease (AD), Creutzfeldt–Jakob disease, and familial prion disease are the most frequent causes of dementia [1, 2]
Dementia is associated with reduced levels of neurotransmitters like acetylcholine. erefore, drugs such as acetylcholinesterase inhibitors, which increase the concentration of acetylcholine in central synapses, are the most suitable choice for treatment. ree AChEIs, donepezil, rivastigmine, and galantamine, have been used to treat mild to moderately severe AD and other types of dementia [4]
D-(-)-Quinic acid supplementation through diet aids in the synthesis of tryptophan and nicotinamide in the gastrointestinal tract (GIT), which leads to an enhancement of DNA repair and nuclear factor kappa B inhibition [7]
Summary
Neurodegenerative diseases such as Alzheimer’s disease (AD), Creutzfeldt–Jakob disease, and familial prion disease are the most frequent causes of dementia [1, 2]. E. Evidence-Based Complementary and Alternative Medicine potential role of D-(-)-quinic acid in dementia has not been evaluated previously but is an interesting candidate as the accumulation of free radicals causes degenerative events associated with aging such as dementia. We hypothesized that D-(-)-quinic acid would prevent the oxidation of free radicals and inhibit the release of inflammatory mediators such as NFκB, TNFα, and NO, which are involved in inflammation and cellular stress. We hypothesized it would help in the inhibition of the monoamine oxidase enzyme (MAO), which is a recently described therapeutic target for dementia
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