|LARSON, JESSICA - Friedman School At Tufts|
|BIELINSKI, DONNA - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|SCHAUSS, ALEXANDER - Aibmr Life Sciences (AMERICAN INSTITUTE FOR BIOSOCIAL AND MEDICAL RESEARCH)|
Submitted to: Journal of Agricultural and Food Chemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/5/2012
Publication Date: 1/5/2012
Citation: Poulose, S.M., Fisher, D.R., Larson, J., Bielinski, D.F., Rimando, A.M., Carey, A.N., Schauss, A.G., Shukitt Hale, B. 2012. Anthocyanin-rich acai (Euterpe oleracea mart.) fruit pulp fractions attenuate inflammatory stress signaling in mouse brain BV-2 microglial cells. Journal of Agricultural and Food Chemistry. 60:1084-1093.
Interpretive Summary: Age-related increases in oxidative stress and inflammation are associated with loss of cognitive and motor functions. Previous research has shown that eating berry fruits can change brain signaling in various areas, including the hippocampus and microglia of animal models. Acai berry is a palm fruit that has similar chemical compounds to berry fruits that may be associated with this change in brain communication. Therefore, we investigated the effect of acai on induced oxidative stress and inflammation in mouse microglial cells by pretreating them with freeze-dried fractions dissolved in four different solvents. All fractions significantly reduced nitrite production induced by lipopolysaccharide (LPS), a known stressor. Several protective mediators were shown to increase in mouse microglial cultures treated with acai. The current study offers valuable insights into the protective effects of acai berry extracts on brain cells, which could have implications for improved cognitive and motor functions.
Technical Abstract: Age-related increases in oxidative stress and inflammation are associated with loss of cognitive and motor functions. Previous research has shown that supplementation with berry fruits can modulate signaling in primary hippocampal neurons or BV-2 mouse microglial cells. Because of the high polyphenolic content, we explored the protective effect of acai berry (Euterpe oleracea Mart) on BV-2 mouse microglial cells. Freeze-dried fractions of acai berry extracted with different polar solvents were applied to BV-2 cells to assess possible cytotoxicity. Except for the ethyl acetate fraction, all the other fractions had no significant cytotoxic effect. The study investigated whether mitigation of oxidative stress and inflammation by acai extracts is due to decreases in nitrite production, inducible nitrous oxide synthase (iNOS) expression and modification of other defensive signals. All fractions significantly reduced the nitrite production induced by lipopolysaccharide (100ng/ml), which was correlated with a significant concentration-dependent decrease in iNOS expression. The protection of microglial cells by acai berry extracts was also accompanied by the significant concentration-dependent reduction in pro-inflammatory mediators such as cyclooxygenase-2, p38 mitogen-activated protein kinase, and transcription factors such as tumor necrosis factor-alpha and nuclear factor kappa-b. The current study offers valuable insights into the protective effects of acai berry extracts on brain cells, which could have implications for improved cognitive and motor functions.