title: Increased oxidative stress is responsible for severer cerebral infarction in stroke-prone spontaneously hypertensive rats.
abstract: OBJECTIVE
  To examine the role of increased oxidative stress in the pathogenesis of cerebral infarction in stroke in stroke-prone spontaneously hypertensive rats (SHR-SP).
  
  
  METHODS
  The differentially expressed brain protein profile was examined in spontaneously hypertensive rats (SHR) (control group) and SHR-SP using two-dimensional fluorescent difference gel electrophoresis (2D-DIGE). In addition, oxidative stress indicators including total antioxidation capacity (TAC), glutathione peroxidase (GPx) activity, and maleic dialdehyde (MDA) were also measured. Lastly, SHR-SP were randomly divided into untreated and treated (vitamins C (200 mg/kg/day) and E (100 mg/kg/day)) groups. After treatment for 4 weeks, half of the animals were sacrificed for detection of TAC, GPx, and MDA. The remaining rats underwent middle cerebral artery occlusion (MCAO) and the infarct areas were measured.
  
  
  RESULTS
  Compared with SHR, the infarct area of SHR-SP was larger (P < 0.01), and the antioxidative proteins including glutathione S-transferase (GST) Pi2 and GST A5 were lower; TAC and GPx activities were decreased and MDA levels. Treatment with vitamins C and E decreased MDA, and increased TAC and GPx activity significantly in SHR-SP, while also decreasing the infarct area (P < 0.01).
  
  
  CONCLUSIONS
  Our findings indicate that oxidative stress plays an important role in the pathogenesis of cerebral ischemia.
authors: Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai, China.
authors: Xiu-Hua
authors: XH
authors: Zhang
authors: Hong
authors: H
authors: Lei
authors: Ai-Jun
authors: AJ
authors: Liu
authors: Ying-Xin
authors: YX
authors: Zou
authors: Fu-Ming
authors: FM
authors: Shen
authors: Ding-Feng
authors: DF
authors: Su
mesh_terms: D000447:Aldehydes / Q000378:metabolism; D000595:Amino Acid Sequence; D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology; D015153:Blotting, Western; D002544:Cerebral Infarction / Q000235:genetics / Q000473:pathology*; D015180:Electrophoresis, Gel, Two-Dimensional; D005979:Glutathione Peroxidase / Q000378:metabolism; D007091:Image Processing, Computer-Assisted; D020244:Infarction, Middle Cerebral Artery / Q000473:pathology; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D013058:Mass Spectrometry; D008969:Molecular Sequence Data; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D020521:Stroke / Q000235:genetics / Q000473:pathology*; D014810:Vitamin E / Q000494:pharmacology; D014815:Vitamins / Q000494:pharmacology
chemical_list: D000447:Aldehydes; D000975:Antioxidants; D009419:Nerve Tissue Proteins; D014815:Vitamins; D014810:Vitamin E; C015977:malealdehyde; D005979:Glutathione Peroxidase; D001205:Ascorbic Acid