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ARS Home » Northeast Area » Boston, Massachusetts » Research » Publications at this Location » Publication #307332
Title: Tart cherry extracts reduce inflammatory stress signaling and enhance calcium buffering in microglial and neuronal cell lines

Author
item Fisher, Derek
item BIELINSKI, DONNA - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item KELLY, MEGAN - Providence College
item Shukitt-Hale, Barbara

Submitted to: Society for Neuroscience Abstracts and Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 6/25/2014
Publication Date: 11/15/2014
Citation: Fisher, D.R., Bielinski, D., Kelly, M.E., Shukitt Hale, B. 2014. Tart cherry extracts reduce inflammatory stress signaling and enhance calcium buffering in microglial and neuronal cell lines. Society for Neuroscience Abstracts and Proceedings 2014. Program #144.18.

Interpretive Summary:

Technical Abstract: Dark-colored fruits, like tart cherries, contain an array of polyphenols that can decrease both inflammation (INF) and oxidative stress (OS). Previous research has shown that supplementation with berry fruits can enhance cognitive and motor function in aged animals. It has been postulated that at least part of the loss of cognitive function in aging may be dependent upon a dysregulation in Ca2+ homeostasis, and that this loss affects numerous signaling pathways. Deficits in Ca2+ buffering (Recovery) induced by OS in hippocampal neurons are antagonized by berry fruit extracts, and berry fruit pretreatment reduces both stress- and inflammatory-induced neuronal dysfunction. A related study in BV-2 mouse microglial cells indicates that at least part of berry fruit-induced reductions in stress-mediated signaling might involve decreases in nitrite (NO) production and inducible nitric oxide synthase (iNOS) expression. Thus, the purpose of the present experiment was to determine if tart cherries, which also improved cognitive behavior in aged rats, would be efficacious in reducing inflammatory stress signaling and enhancing calcium buffering in microglial and neuronal cell lines. Rat microglial (HAPI) cells were pretreated for 1-6 hours with cherry extract (0-1.0mg/ml), treated with 0 or 100ng/ml lipopolysaccharide (LPS) overnight, and assessed for changes in nitric oxide production and iNOS expression. Cherry concentration-dependently reduced LPS-induced nitric oxide production in HAPI microglia; however, higher doses and longer treatment durations negatively affected cell viability. The effects of the cherry extract on LPS-induced TNF-alpha and COX-2 production are currently being assessed. Cherry was also effective in preventing dopamine (DA) stress-induced loss of Ca2+ buffering at similar concentrations. Therefore, tart cherries, like other dark-colored fruits we have assessed, may be effective in reducing inflammatory stress-mediated signals and preventing oxidative stress-induced calcium dysregulation.