PMID- 24563435
OWN - NLM
STAT- MEDLINE
DCOM- 20150402
LR  - 20140224
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 18
IP  - 3
DP  - 2014
TI  - Oxidative stress in rats with hyperhomo-cysteinemia and intervention effect of 
      lutein.
PG  - 359-64
LID - 6632 [pii]
AB  - AIM: The current study aims to explore the possible molecular mechanism of 
      hyperhomocysteinemia (HHcy) mediated atherosclerosis (AS) and to find an 
      effective intervention method for AS. MATERIALS AND METHODS: A total of 40 Wistar 
      rats were equalized into four groups: blank control, HHcy, folacin intervention, 
      and lutein intervention groups. HHcy rat models were established. The 
      intervention groups were respectively lavaged with folacin and lutein. Oxidative 
      stress states, the levels of nitric oxide (NO) and endothelin-1 (ET-1), as well 
      as the expression of nuclear factor (NF)-kappaB p65 and intercellular adhesion 
      molecule (ICAM)-1 were compared. RESULTS: In the HHcy rats, the activity of serum 
      superoxide dismutase (SOD) and glutathione peroxidase (GPx) significantly 
      decreased, whereas the malondialdehyde content and hydroxyl radical level 
      noticeably increased, indicating that the rats stayed in aggravated oxidative 
      stress states. Lutein intervention inhibited HHcy-induced oxidative stress 
      excitement. In the HHcy rats, the NO level significantly decreased, whereas the 
      ET-1 level significantly increased, indicating that HHcy mediated vascular 
      endothelial dysfunction. Lutein reversed such dysfunction. In the HHcy rats, the 
      mRNA and protein expression of SOD2 and GPX1 in the aortic wall tissue decreased, 
      whereas that of NF-kappaB p65 and ICAM-1 increased. Lutein significantly upregulated 
      the mRNA and protein expression of SOD2 and GPx1 and downregulated the expression 
      of NF-kappaB p65 and ICAM-1. CONCLUSIONS: Oxidative stress and inflammation are the 
      important mechanisms of HHcy-mediated AS. In particular, HHcy-induced aggravated 
      oxidative stress may function as the initial AS-mediating mechanism, upregulating 
      the expression of NF-kappaB p65 and ICAM-1 and thereby becoming associated with AS. 
      Lutein noticeably intervenes in and inhibits Hcy-mediated oxidative stress 
      excitement and downregulates the expression of inflammation-associated 
      informational molecules.
FAU - Wang, S
AU  - Wang S
AD  - Department of Cardiology , the First Affiliated Hospital and Department of 
      Biochemistry, School of Basic Medicine of Zhengzhou University, Zhengzhou, China. 
      zjdocchina@163.com  
FAU - Wang, M
AU  - Wang M
FAU - Zhang, S
AU  - Zhang S
FAU - Zhao, L
AU  - Zhao L
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Antioxidants)
RN  - 0 (Transcription Factor RelA)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - X72A60C9MT (Lutein)
SB  - IM
MH  - Animals
MH  - Antioxidants/administration & dosage/*therapeutic use
MH  - Atherosclerosis/etiology/immunology/metabolism/*prevention & control
MH  - Disease Models, Animal
MH  - Down-Regulation
MH  - Endothelium, Vascular/drug effects/immunology/metabolism
MH  - Hyperhomocysteinemia/complications/*drug therapy/immunology/metabolism
MH  - Intercellular Adhesion Molecule-1/biosynthesis
MH  - Lutein/administration & dosage/*therapeutic use
MH  - Male
MH  - Oxidative Stress/*drug effects
MH  - Rats, Wistar
MH  - Transcription Factor RelA/biosynthesis
EDAT- 2014/02/25 06:00
MHDA- 2015/04/04 06:00
CRDT- 2014/02/25 06:00
PHST- 2014/02/25 06:00 [entrez]
PHST- 2014/02/25 06:00 [pubmed]
PHST- 2015/04/04 06:00 [medline]
AID - 6632 [pii]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2014;18(3):359-64.