Darkroom/Safelight LED Lamps; Page 2, Series BSD-1293, BSD-1260

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BB and Inflammation

Itinerary - View Abstract: "Abstract View
INHIBITORY EFFECTS OF BLUEBERRY POLYPHENOLS ON THE PRODUCTION OF PROINFLAMMATORY MEDIATORS IN ACTIVATED MICROGLIAL CELLS
F.C.Lau*; D.F.Bielinski; J.A.Joseph
Neuroscience Laboratory, USDA, HNRCA at Tufts, Boston, MA, USA
Microglia are the major protectors of the immune system in the central nervous system (CNS). Acutely activated microglia, by brain injury or infection, produce cellular and metabolic alterations that are beneficial to the microenvironment of the CNS. However, pathological activation of microglia has been demonstrated to contribute to the progressive damage in neurodegenerative diseases such as stroke, Alzheimers disease (AD), multiple sclerosis (MS) and human immunodeficiency virus (HIV)-associated dementia. This occurs via the sustained up-regulation of microglial genes to inflammation and the generation of various proinflammatory mediators including nitric oxide (NO), tumor necrosis factor-alpha (TNF-), and interleukin-1 beta (IL-1). Blueberries are rich in anthocyanins, which are among the plant polyphenols that have potent antioxidant and anti-inflammatory activities. The current study showed that treatment with blueberry (BB) extracts significantly and dose-dependently reduced the lipopolysaccharide (LPS)-induced NO production in conditioned media from BV2 murine microglial cells. Reactive oxygen species (ROS) release was also reduced in BB-treated LPS-activated BV2 cells. In addition, BB extracts significantly attenuated the protein expression of the inducible NO synthase (iNOS), cyclo-oxygenases 2 (COX-2), and the pre-processed form of IL-1 in the LPS-activated BV2 cells. Furthermore, the secretion of the inflammatory cytokines IL-1 and TNF- into the conditioned media from the LPS-activated BV2 cells was inhibited by BB treatment. The results from this study suggest that BB polyphenols attenuate inflammatory responses of the brain microglial cells a"

BB and Hippocampus

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BLUEBERRY EXTRACT IMPROVES SURVIVAL OF GRAFTED HIPPOCAMPAL FORMATION: BIOLOGICAL MECHANISMS
L.M.Willis1*; C.D.Umphlet1; V.Zaman1; A.Moore1; P.C.Bickford3; A.C.Granholm1,2
1. Dept Neurosciences, 2. Center on Aging, Med. Univ. of South Carolina, Charleston, SC, USA
3. Dept. Neurosurgery, Univ. of South Florida, Tampa, FL, USA
Dietary supplementation with foods high in antioxidants, such as blueberries, has been shown to improve memory and increase neurogenesis in the hippocampus of aged rats. In addition to their potent antioxidant properties, blueberries have been shown to decrease mRNA for the pro-inflammatory cytokine TNF in certain brain regions. Considering that oxidative stress and inflammation can both be detrimental to the survival of grafted neural tissue, the present study focused on biological mechanisms of blueberry extract in terms of improving graft survival in an intraocular grafting paradigm. Graft recipients were given either a control diet or a diet that had been supplemented with 2% blueberry extract one week prior to transplantation and were maintained on the respective diets for the duration of the study. Fetal hippocampal tissue (E18) was transplanted to the anterior eye chamber of young adult (6 mo) and middle-aged (19 mo) recipients. Fetal hippocampal grafts to middle-aged hosts exhibited poor survival, less overall growth, and reduced organization. When middle-aged graft recipients were maintained on a diet with blueberry extract, survival of hippocampal intraocular grafts was greatly improved: size and cellular organization of grafts was comparable to that seen in tissue grafted to young recipients. Preliminary results indicate that blueberries may enhance neo-vascularization and reduce inflammation following the ocular surgery. Thus, our preliminary data indicate that the active ingredients of this nutraceutical may provide various neuroprotective"

BB and hippocampus

Itinerary - View Abstract: "Abstract View
BLUEBERRY EXTRACT INHIBITS DA-OR A-INDUCED DECREMENTS IN CALCIUM FLUX IN PRIMARY HIPPOCAMPAL CELLS
J.A.Joseph*; D.R.Fisher
1. Human Nutrit. Res. Center on Aging, 2. Neuroscience, Tufts Univ., Boston, MA, USA
Previously, we have shown that when exposed to dopamine (DA) or amyloid beta (A) COS-7 cells transfected with muscarinic receptor (MAChR) subtypes (M1, M2, or M4) lose their ability to buffer or extrude calcium following oxotremorine-induced depolarization. However, pre-treatment of these cells with a high antioxidant/anti-inflammatory blueberry extract (BB) prevented the DA or A effects on calcium buffering. Similarly, it also appears that dietary BB also reversed several parameters of neuronal and behavioral aging in rodents, including cognitive function. It has been postulated that at least part of the loss of cognitive function in aging may be dependent upon a dysregulation in calcium homeostasis, and this loss affects numerous downstream signaling pathways that could ultimately affect learning and memory. Present experiments were carried out to determine the role of oxidative stress in this calcium regulation by assessing whether: a) calcium buffering would be altered in DA- or A-exposed cultured primary hippocampal neuronal cells (HNC) and b) BB or BB polyphenolic pretreatment of the cells would prevent these deficits. Thus, control or BB (0.5mg/ml)-treated HNC were exposed to 0, 0.1mM DA or 100M A and Ca2+ buffering (Ca2+ recovery time, Ca2+RT, following KCl) was then carried out on the cells prior to and following the KCl-induced depolarization. Ca2+RT was assessed as the % of HNC showing recovery to 50%-70% of control at 5, 10, or 15 min after depolarization. Results indicated that DA significantly lowered Ca2+RT in the HNC at all times examined after depolarization. However, BB-treatment prevented these declines to 50%-60% of control, especially at the 10 and 1"

BLUEBERRY

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DIFFERENTIAL EFFECTS OF BLUEBERRY EXTRACT PREPARATIONS ON COGNTIVE AND MOTOR FUNCTION IN AGING: THE ROLE OF PHENOLICS
B.Shukitt-Hale1*; A.N.Carey1; W.Kalt2; J.McDonald2; M.Vinqvist2; J.A.Joseph1
1. USDA, ARS, Human Nutritrition Research Ctr. on Aging, Boston, MA, USA
2. Agriculture and Agri-food Canada, Kentville, NS, Canada
We have shown that whole, crude blueberry (BB) extracts are able to reverse several parameters of brain aging (e.g., deficits in cell communication) as well as age-related motor and cognitive deficits when fed to rats from 19-21 months of age. These effects appear to be the result of compounds (polyphenolics) that enhance the survivability of the plant, possibly through direct effects on brain signaling or indirectly through their antioxidant and anti-inflammatory properties. However, given the complex mixtures of phytochemicals in fruits, it is difficult to discern from a crude BB extract the contribution of non-polyphenolic compounds to these effects. Thus, the present study examined 3 different BB-derived diets, all equated on phenolic level, to determine whether the effects observed with the whole, crude BB extract are indeed due to polyphenolics or whether other compounds were contributing to the age-related improvements in behavior. Old (19 mo) F344 rats were fed a control diet or one with 5.4% crude BB extract (as before), a 2% pre-C18 column BB extract, or a 0.1% post-C18 column semi-purified BB extract (a mixture of only BB phenolics with the sugars and organic acids removed) for 8 weeks prior to motor and cognitive testing. Results showed that only the crude BB extract diet improved rotarod performance, while all three BB-derived diets improved working memory in the MWM. Therefore, phenolics are important components in the beneficial effects of BBs on age-related improvements in cognition, but other compounds may play a role in motor improveme"

IngentaConnect Preventive actions of a synthetic antioxidant in a novel animal m...

IngentaConnect Preventive actions of a synthetic antioxidant in a novel animal m...: "Preventive actions of a synthetic antioxidant in a novel animal model of AIDS dementia

Authors: Bjugstad K.B.; Flitter W.D.; Garland W.A.; Su G.C.; Arendash G.W.1

Source: Brain Research, Volume 795, Number 1, 8 June 1998, pp. 349-357(9)

Publisher: Elsevier Science
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Abstract:

Accumulating evidence indicates that the mechanism for causing AIDS dementia complex (ADC) involves the release of damaging inflammatory-related agents by HIV-infected microglia in the brain resulting in CNS oxidative damage. One such agent, tumor necrosis factor alpha (TNF-alpha) is consistently elevated in the brains of ADC patients compared to non-demented HIV patients. To model this aspect of ADC in rats, chronic ventricular infusions of TNF-alpha were given and found to induce several aspects of ADC, including weight loss, learning/memory impairment, enlarged lateral ventricles, and increased apoptosis. Concurrent oral treatment with the antioxidant CPI-1189 prevented all of these TNF-alpha induced effects. The results support TNF-alpha as a key toxic agent in ADC and provide the first in vivo evidence that chronic treatment with a synthetic antioxidant may protect HIV-infected patients against ADC. Our findings may also have implications in other neurological diseases where brain TNF-alpha levels are elevated and inflammation/oxidative stress is suspected to be a contributing cause, such as Alzheimer's disease and Parkinson's disease.

Keywords: AIDS dementia complex; Inflammation; '>Tumor necrosis factor-alpha; Antioxidant; Apoptosis; Memory impairment"

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