PMID- 23782872
OWN - NLM
STAT- MEDLINE
DCOM- 20131105
LR  - 20211021
IS  - 1742-2094 (Electronic)
IS  - 1742-2094 (Linking)
VI  - 10
DP  - 2013 Jun 19
TI  - Nutraceutical agents with anti-inflammatory properties prevent dietary 
      saturated-fat induced disturbances in blood-brain barrier function in wild-type 
      mice.
PG  - 73
LID - 10.1186/1742-2094-10-73 [doi]
AB  - BACKGROUND: Emerging evidence suggests that disturbances in the blood-brain 
      barrier (BBB) may be pivotal to the pathogenesis and pathology of vascular-based 
      neurodegenerative disorders. Studies suggest that heightened systemic and central 
      inflammations are associated with BBB dysfunction. This study investigated the 
      effect of the anti-inflammatory nutraceuticals garlic extract-aged (GEA), alpha 
      lipoic acid (ALA), niacin, and nicotinamide (NA) in a murine dietary-induced 
      model of BBB dysfunction. METHODS: C57BL/6 mice were fed a diet enriched in 
      saturated fatty acids (SFA, 40% fat of total energy) for nine months to induce 
      systemic inflammation and BBB disturbances. Nutraceutical treatment groups 
      included the provision of either GEA, ALA, niacin or NA in the positive control 
      SFA-group and in low-fat fed controls. Brain parenchymal extravasation of plasma 
      derived immunoglobulin G (IgG) and large macromolecules (apolipoprotein (apo) B 
      lipoproteins) measured by quantitative immunofluorescent microscopy, were used as 
      markers of disturbed BBB integrity. Parenchymal glial fibrillar acidic protein 
      (GFAP) and cyclooxygenase-2 (COX-2) were considered in the context of surrogate 
      markers of neurovascular inflammation and oxidative stress. Total anti-oxidant 
      status and glutathione reductase activity were determined in plasma. RESULTS: 
      Brain parenchymal abundance of IgG and apoB lipoproteins was markedly exaggerated 
      in mice maintained on the SFA diet concomitant with significantly increased GFAP 
      and COX-2, and reduced systemic anti-oxidative status. The nutraceutical GEA, 
      ALA, niacin, and NA completely prevented the SFA-induced disturbances of BBB and 
      normalized the measures of neurovascular inflammation and oxidative stress. 
      CONCLUSIONS: The anti-inflammatory nutraceutical agents GEA, ALA, niacin, or NA 
      are potent inhibitors of dietary fat-induced disturbances of BBB induced by 
      systemic inflammations.
FAU - Takechi, Ryusuke
AU  - Takechi R
AD  - School of Public Health, Curtin Health Innovation Research Institute, Biosciences 
      Research Precinct, Faculty of Health Sciences, Curtin University, Kent st, 
      Bentley, WA, 6102, Australia.
FAU - Pallebage-Gamarallage, Menuka M
AU  - Pallebage-Gamarallage MM
FAU - Lam, Virginie
AU  - Lam V
FAU - Giles, Corey
AU  - Giles C
FAU - Mamo, John C
AU  - Mamo JC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130619
PL  - England
TA  - J Neuroinflammation
JT  - Journal of neuroinflammation
JID - 101222974
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Apolipoproteins A)
RN  - 0 (Dietary Fats)
RN  - 0 (Fatty Acids)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Lipids)
RN  - 2679MF687A (Niacin)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/*pharmacology
MH  - Apolipoproteins A/metabolism
MH  - Blood-Brain Barrier/*drug effects/physiology
MH  - Cyclooxygenase 2/metabolism
MH  - *Diet
MH  - Dietary Fats/*pharmacology
MH  - *Dietary Supplements
MH  - Fatty Acids/*pharmacology
MH  - Female
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Immunoglobulin G/metabolism
MH  - Inflammation/pathology
MH  - Lipids/blood
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microscopy, Fluorescence
MH  - Niacin/pharmacology
MH  - Oxidative Stress/physiology
MH  - Weight Gain/physiology
PMC - PMC3693897
EDAT- 2013/06/21 06:00
MHDA- 2013/11/06 06:00
PMCR- 2013/06/19
CRDT- 2013/06/21 06:00
PHST- 2012/12/21 00:00 [received]
PHST- 2013/06/08 00:00 [accepted]
PHST- 2013/06/21 06:00 [entrez]
PHST- 2013/06/21 06:00 [pubmed]
PHST- 2013/11/06 06:00 [medline]
PHST- 2013/06/19 00:00 [pmc-release]
AID - 1742-2094-10-73 [pii]
AID - 10.1186/1742-2094-10-73 [doi]
PST - epublish
SO  - J Neuroinflammation. 2013 Jun 19;10:73. doi: 10.1186/1742-2094-10-73.