PMID- 17955498
OWN - NLM
STAT- MEDLINE
DCOM- 20080828
LR  - 20121115
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 103
IP  - 6
DP  - 2008 Apr 15
TI  - Astaxanthin protects mesangial cells from hyperglycemia-induced oxidative 
      signaling.
PG  - 1925-37
AB  - Astaxanthin (ASX) is a carotenoid that has potent protective effects on diabetic 
      nephropathy in mice model of type 2 diabetes. In this study, we investigated the 
      protective mechanism of ASX on the progression of diabetic nephropathy using an 
      in vitro model of hyperglycemia, focusing on mesangial cells. Normal human 
      mesangial cells (NHMCs) were cultured in the medium containing normal (5 mM) or 
      high (25 mM) concentrations of D-glucose. Reactive oxygen species (ROS) 
      production, the activation of nuclear transcription factors such as nuclear 
      factor kappa B (NFkappaB) and activator protein-1 (AP-1), and the 
      expression/production of transforming growth factor-beta 1 (TGFbeta(1)) and 
      monocyte chemoattractant protein-1 (MCP-1) were evaluated in the presence or 
      absence of ASX. High glucose (HG) exposure induced significant ROS production in 
      mitochondria of NHMCs, which resulted in the activation of transcription factors, 
      and subsequent expression/production of cytokines that plays an important role in 
      the mesangial expansion, an important event in the pathogenesis of diabetic 
      nephropathy. ASX significantly suppressed HG-induced ROS production, the 
      activation of transcription factors, and cytokine expression/production by NHMCs. 
      In addition, ASX accumulated in the mitochondria of NHMCs and reduced the 
      production of ROS-modified proteins in mitochondria. ASX may prevent the 
      progression of diabetic nephropathy mainly through ROS scavenging effect in 
      mitochondria of mesangial cells and thus is expected to be very useful for the 
      prevention of diabetic nephropathy.
FAU - Manabe, Emiko
AU  - Manabe E
AD  - School of Nursing, Kyoto Prefectural University of Medicine, Kyoto 602-8566, 
      Japan.
FAU - Handa, Osamu
AU  - Handa O
FAU - Naito, Yuji
AU  - Naito Y
FAU - Mizushima, Katsura
AU  - Mizushima K
FAU - Akagiri, Satomi
AU  - Akagiri S
FAU - Adachi, Satoko
AU  - Adachi S
FAU - Takagi, Tomohisa
AU  - Takagi T
FAU - Kokura, Satoshi
AU  - Kokura S
FAU - Maoka, Takashi
AU  - Maoka T
FAU - Yoshikawa, Toshikazu
AU  - Yoshikawa T
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (Xanthophylls)
RN  - 8XPW32PR7I (astaxanthine)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Cell Line
MH  - Chemokine CCL2/metabolism
MH  - Diabetic Neuropathies/etiology/metabolism/*prevention & control
MH  - Humans
MH  - Hyperglycemia/complications/*metabolism
MH  - Mesangial Cells/*drug effects/metabolism
MH  - Mitochondria/metabolism
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - NF-kappa B/metabolism
MH  - Oxidation-Reduction
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction
MH  - Transcription Factor AP-1/metabolism
MH  - Transforming Growth Factor beta1/metabolism
MH  - Xanthophylls/pharmacology
EDAT- 2007/10/24 09:00
MHDA- 2008/08/30 09:00
CRDT- 2007/10/24 09:00
PHST- 2007/10/24 09:00 [pubmed]
PHST- 2008/08/30 09:00 [medline]
PHST- 2007/10/24 09:00 [entrez]
AID - 10.1002/jcb.21583 [doi]
PST - ppublish
SO  - J Cell Biochem. 2008 Apr 15;103(6):1925-37. doi: 10.1002/jcb.21583.