Nifedipine treatment reduces brain damage after transient focal ischemia, possibly through its antioxidative effects

Mayumi Yamato, Takeshi Shiba, Tomomi Ide, Youhei Honda, Ken Ichi Yamada, Hiroyuki Tsutsui

研究成果: ジャーナルへの寄稿記事

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Stroke is a major cause of mortality and morbidity in hypertensive patients. This study investigated the effects of nifedipine, an L-type voltage-gated Ca 2+ channel blocker, on ischemic lesion volume after focal cerebral ischemia and reperfusion in rats. Rats were subjected to 1 h of transient middle cerebral artery occlusion (MCAO). At 2 days after MCAO, the rats were randomized into two groups that were fed either a normal control diet (n=10) or a nifedipine (0.001%) containing diet (n=11) for 2 weeks. Nifedipine treatment significantly reduced ischemic lesion volume (116.5±10.8 vs. 80.0±8.2 mm 3, P<0.05) without affecting body weight or blood pressure. It also decreased thiobarbituric-reactive substances, an index of lipid peroxide, (2.6±0.4 vs. 1.7±0.1 mol g -1 tissue, P<0.05) and increased glutathione peroxidase (54.9±4.7 vs. 70.9±6.4 U g -1 protein, P<0.05) and glutathione reductase activities (32.4±1.4 vs. 39.9±2.7 U g -1 protein, P<0.05) in the mitochondria from the ischemic hemispheres. These results suggest that nifedipine treatment can reduce ischemic lesion volume after focal cerebral ischemia, possibly because of the decrease in oxidative stress with an increase in antioxidant activities within the ischemic area.

元の言語英語
ページ(範囲)840-845
ページ数6
ジャーナルHypertension Research
34
発行部数7
DOI
出版物ステータス出版済み - 7 1 2011

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All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

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