PMID- 16166554
OWN - NLM
STAT- MEDLINE
DCOM- 20051207
LR  - 20131121
IS  - 1524-4571 (Electronic)
IS  - 0009-7330 (Linking)
VI  - 97
IP  - 9
DP  - 2005 Oct 28
TI  - Protective effect of alpha-lipoic acid in lipopolysaccharide-induced endothelial 
      fractalkine expression.
PG  - 880-90
AB  - Fractalkine is a unique chemokine that functions as a chemoattractant as well as 
      an adhesion molecule on endothelial cells activated by proinflammatory cytokines. 
      Alpha-lipoic acid (LA), a naturally occurring dithiol compound, is an essential 
      cofactor for mitochondrial bioenergetic enzymes. LA improves glycemic control, 
      reduces diabetic polyneuropathies, and mitigates toxicity associated with heavy 
      metal poisoning. The effects of LA on processes associated with sepsis, however, 
      are unknown. We evaluated the antiinflammatory effect of LA on fractalkine 
      expression in a lipopolysaccharide-induced endotoxemia model. Tumor necrosis 
      factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) significantly induced 
      fractalkine mRNA and protein expression in endothelial cells. LA strongly 
      suppressed TNF-alpha- or IL-1beta-induced fractalkine expression in endothelial 
      cells by suppressing the activities of nuclear factor-kappaB and specificity 
      protein-1. LA also decreased TNF-alpha- or IL-1beta-stimulated monocyte adhesion 
      to human umbilical vein endothelial cells. As shown by immunohistochemistry, 
      fractalkine protein expression was markedly increased by treatment with 
      lipopolysaccharide in arterial endothelial cells, endocardium, and endothelium of 
      intestinal villi. LA suppressed lipopolysaccharide-induced fractalkine protein 
      expression and infiltration of endothelin 1-positive cells into the heart and 
      intestine in vivo. LA protected against lipopolysaccharide-induced myocardial 
      dysfunction and improved survival in lipopolysaccharide-induced endotoxemia. 
      These results suggest that LA could be an effective agent to reduce 
      fractalkine-mediated inflammatory processes in endotoxemia.
FAU - Sung, Mi Jeong
AU  - Sung MJ
AD  - Department of Internal Medicine, Research Institute of Clinical Medicine, Chonbuk 
      National University Medical School, Jeonju, 560-180, Korea.
FAU - Kim, Won
AU  - Kim W
FAU - Ahn, So Young
AU  - Ahn SY
FAU - Cho, Chung-Hyun
AU  - Cho CH
FAU - Koh, Gou Young
AU  - Koh GY
FAU - Moon, Sang-Ok
AU  - Moon SO
FAU - Kim, Duk Hoon
AU  - Kim DH
FAU - Lee, Sik
AU  - Lee S
FAU - Kang, Kyung Pyo
AU  - Kang KP
FAU - Jang, Kyu Yun
AU  - Jang KY
FAU - Park, Sung Kwang
AU  - Park SK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20050915
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (CX3CL1 protein, human)
RN  - 0 (Chemokine CX3CL1)
RN  - 0 (Chemokines, CX3C)
RN  - 0 (Cx3cl1 protein, rat)
RN  - 0 (EDA protein, human)
RN  - 0 (Ectodysplasins)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Membrane Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Sp1 Transcription Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 73Y7P0K73Y (Thioctic Acid)
SB  - IM
MH  - Animals
MH  - Blood Pressure/drug effects
MH  - Cell Adhesion/drug effects
MH  - Cells, Cultured
MH  - Chemokine CX3CL1
MH  - Chemokines, CX3C/*genetics
MH  - Ectodysplasins
MH  - Endothelial Cells/*metabolism
MH  - Endotoxemia/drug therapy
MH  - Humans
MH  - Interleukin-1/pharmacology
MH  - Lipopolysaccharides/*toxicity
MH  - Male
MH  - Membrane Proteins/analysis/*genetics
MH  - Monocytes/drug effects
MH  - Myocardium/pathology
MH  - NF-kappa B/metabolism
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sp1 Transcription Factor/metabolism
MH  - Thioctic Acid/*pharmacology
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 2005/09/17 09:00
MHDA- 2005/12/13 09:00
CRDT- 2005/09/17 09:00
PHST- 2005/09/17 09:00 [pubmed]
PHST- 2005/12/13 09:00 [medline]
PHST- 2005/09/17 09:00 [entrez]
AID - 01.RES.0000186522.89544.4D [pii]
AID - 10.1161/01.RES.0000186522.89544.4D [doi]
PST - ppublish
SO  - Circ Res. 2005 Oct 28;97(9):880-90. doi: 10.1161/01.RES.0000186522.89544.4D. Epub 
      2005 Sep 15.