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CNS Neurosci Ther. 2011 Dec;17(6):590-8. doi: 10.1111/j.1755-5949.2011.00271.x.

Increased oxidative stress is responsible for severer cerebral infarction in stroke-prone spontaneously hypertensive rats.

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  • 1Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai, China.

Abstract

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.

© 2011 Blackwell Publishing Ltd.

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PMID:
22117799
[PubMed - indexed for MEDLINE]
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