Modulation of oxidative stress, inflammation, autophagy and expression of Nrf2 in hippocampus and frontal cortex of rats fed with acai-enriched diets

Authors: POULOSE, SHIBU - Jean Mayer Human Nutrition Research Center On Aging At Tufts University; BIELINSKI, DONNA - Jean Mayer Human Nutrition Research Center On Aging At Tufts University; CAREY, AMANDA - Simmons College; SCHAUSS, ALEXANDER - Aibmr Life Sciences (AMERICAN INSTITUTE FOR BIOSOCIAL AND MEDICAL RESEARCH); Shukitt-Hale, Barbara

Submitted to: Nutritional Neuroscience
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/24/2015
Publication Date: 1/11/2016
Citation: Poulose, S.M., Bielinski, D.F., Carey, A., Schauss, A.G., Shukitt Hale, B. 2016. Modulation of oxidative stress, inflammation, autophagy and expression of Nrf2 in hippocampus and frontal cortex of rats fed with acai-enriched diets. Nutritional Neuroscience. doi: 10.1080/1028415X.2015.1125654.

Interpretive Summary: Acai, an exotic palm fruit, has recently emerged as a promising source of natural antioxidants with wide pharmacological and nutritional value. In this study, two different species of acai, naturally grown in two distinct regions of the Amazon, Brazilian and Bolivian, were studied for their effects on brain health and mental processes. Chemical analyses were performed in critical brain regions associated with memory and mental processing of 19-month-old acai-fed rats, in which the mental-processing benefits of acai had been established. Results indicated significant reductions in the levels of brain molecules known to cause cellular stress and inflammation in acai-fed rats. In addition, increases in the levels of brain- originating antioxidants (molecules involved in counteracting stress and inflammation), as well as molecules responsible for their production, were found in the brains of the acai-fed rats. Furthermore, analysis of molecules involved in cellular clearance of toxic, damaged molecules revealed an increase in these “housekeeping” molecules in the acai-fed rats. In general, results were more positive for one species of acai (the one from the Bolivian Amazon) over the other. Therefore, an acai-enriched diet might modulate a number of cellular pathways, counteracting stress, reducing inflammation, and stimulating clearance of toxic molecules which might lead to improvement in cognitive function of the aging brain.

Technical Abstract: Acai (Euterpe spp.), an exotic palm fruit, has recently emerged as a promising source of natural antioxidants with wide pharmacological and nutritional value. In this study, two different species of acai pulp extracts, naturally grown in two distinct regions of the Amazon, namely, Euterpe oleracea Mart. (habitat: Brazilian floodplains of the Amazon) and Euterpe precatoria Mart. (habitat: Bolivian Amazon), were studied for their effects on brain health and cognition. Neurochemical analyses were performed in critical brain regions associated with memory and cognition of 19 month old acai-fed rats, in whom the cognitive benefits of acai had been established. Results indicated significant reductions (p<0.05) in prooxidant NADPH-oxidoreductase-2 (NOX2) and proinflammatory transcription factor NF-kappa B in acai-fed rats. Measurement of Nrf2 expression, a transcription factor for antioxidant enzymes, and a possible link between oxidative stress, neuroinflammation and autophagy mechanisms, indicated significant overexpression (p<0.005) in the hippocampus and frontal cortex of the acai-fed rats. Furthermore, significant activation of endogenous antioxidant enzymes GST and SOD were also observed in the acai-fed animals when compared to control. Analysis of autophagy markers such as p62, phospho-mTOR, beclin1 and MAP1B-LC3 revealed differential expression in frontal cortex and hippocampus, mostly indicating an upregulation in the acai-fed rats. In general, results were more profound for EP than EO in hippocampus as well as frontal cortex. Therefore, an acai-enriched diet could possibly modulate Nrf2, which is known to modulate the intracellular redox status, thereby regulating the ubiquitin-proteosomal pathway, ultimately affecting cognitive function in the aging brain.