Increased Oxidative Stress Is Responsible for Severer Cerebral Infarction in Stroke‐Prone Spontaneously Hypertensive Rats

• Published in: CNS neuroscience & therapeutics 2011-12, Vol.17 (6), p.590-598
• Main Authors: Zhang, Xiu‐Hua, Lei, Hong, Liu, Ai‐Jun, Zou, Ying‐Xin, Shen, Fu‐Ming, Su, Ding‐Feng
• Format: Article
• Language: English
• Subjects: Aldehydes - metabolism; Amino Acid Sequence; Animals; Antioxidants - metabolism; Antioxidants - pharmacology; Ascorbic acid; Ascorbic Acid - pharmacology; Biological and medical sciences; Blotting, Western; Brain; Central nervous system; Cerebral blood flow; Cerebral infarction; Cerebral Infarction - genetics; Cerebral Infarction - pathology; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Electrophoresis, Gel, Two-Dimensional; Gel electrophoresis; Glutathione peroxidase; Glutathione Peroxidase - metabolism; Glutathione transferase; Image Processing, Computer-Assisted; Infarction, Middle Cerebral Artery - pathology; Ischemia; Lipid Peroxidation - physiology; Male; Mass Spectrometry; Medical sciences; Molecular Sequence Data; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis; Nerve Tissue Proteins - biosynthesis; Nervous system; Neurology; Oxidative stress; Oxidative Stress - physiology; Pathogenesis; Rats; Rats, Inbred SHR; Spontaneously hypertensive rats; Stroke; Stroke - genetics; Stroke - pathology; Stroke‐prone spontaneously hypertensive rats; Two‐dimensional fluorescent difference gel electrophoresis; Vascular diseases and vascular malformations of the nervous system; Vitamin E - pharmacology; Vitamins - pharmacology
• ISSN: 1755-5930; 1755-5949
• DOI: 10.1111/j.1755-5949.2011.00271.x

SUMMARY Aims: 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.