PMID- 20643106
OWN - NLM
STAT- MEDLINE
DCOM- 20100902
LR  - 20100816
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 399
IP  - 1
DP  - 2010 Aug 13
TI  - Dietary restriction suppresses inflammation and delays the onset of stroke in 
      stroke-prone spontaneously hypertensive rats.
PG  - 98-103
LID - 10.1016/j.bbrc.2010.07.048 [doi]
AB  - Subjects with high blood levels of inflammatory markers and patients with chronic 
      inflammatory disorders are at high risk for stroke. Dietary restriction (DR) 
      suppresses systemic inflammation to deter age-related chronic diseases. To 
      examine whether DR delays the onset of stroke, 10-week-old stroke-prone 
      spontaneously hypertensive rats (SHRSP) were assigned to either a control (ad 
      libitum) or DR (50% diet of control) group, and day of stroke onset and lifespan 
      were observed. DR markedly delayed the onset of stroke in SHRSP compared to 
      control without affecting blood pressure. Day of stroke onset (median) in the 
      control group was 34days, whereas it was 70days in the DR group. After 2weeks of 
      DR and before the onset of stroke, plasma levels of interleukin-1beta (IL-1beta), 
      tumor necrosis factor-alpha (TNF-alpha), and monocyte chemoattractant protein-1 
      (MCP-1) and their mRNA expression levels in adipose tissue were significantly 
      lower in the DR rats than in the control rats. Intercellular adhesion molecule-1 
      (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) mRNA expression levels in 
      cerebrovascular endothelial cells (CVECs), and macrophage infiltration into brain 
      were lower in the DR rats than in the control rats. IL-1beta and TNF-alpha 
      treatment in CVECs increased MCP-1, C-reactive protein, ICAM-1, and VCAM-1 mRNA 
      and their protein levels in vitro. In conclusion, suppression of inflammation in 
      response to DR may lead to a delay in the onset of stroke independent of any 
      effect on blood pressure in SHRSP.
CI  - 2010 Elsevier Inc. All rights reserved.
FAU - Chiba, Tsuyoshi
AU  - Chiba T
AD  - National Institute of Health and Nutrition, Shinjuku-ku, Tokyo, Japan. 
      tyschiba@nih.go.jp
FAU - Ezaki, Osamu
AU  - Ezaki O
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100717
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Adipose Tissue/*metabolism
MH  - Animals
MH  - Blood Pressure
MH  - Chemokine CCL2/metabolism
MH  - *Diet
MH  - Inflammation/*diet therapy/metabolism
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Interleukin-1beta/metabolism
MH  - Male
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Stroke/*prevention & control
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Vascular Cell Adhesion Molecule-1/metabolism
EDAT- 2010/07/21 06:00
MHDA- 2010/09/03 06:00
CRDT- 2010/07/21 06:00
PHST- 2010/07/06 00:00 [received]
PHST- 2010/07/14 00:00 [accepted]
PHST- 2010/07/21 06:00 [entrez]
PHST- 2010/07/21 06:00 [pubmed]
PHST- 2010/09/03 06:00 [medline]
AID - S0006-291X(10)01359-8 [pii]
AID - 10.1016/j.bbrc.2010.07.048 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2010 Aug 13;399(1):98-103. doi: 
      10.1016/j.bbrc.2010.07.048. Epub 2010 Jul 17.