title: Nifedipine treatment reduces brain damage after transient focal ischemia, possibly through its antioxidative effects.
abstract: 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 μmol 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.
authors.affiliation: 1] Department of REDOX Medicinal Science, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan. yamato68@redoxnavi.med.kyushu-u.ac.jp
authors.forename: Mayumi
authors.initials: M
authors.lastname: Yamato
authors.forename: Takeshi
authors.initials: T
authors.lastname: Shiba
authors.forename: Tomomi
authors.initials: T
authors.lastname: Ide
authors.forename: Youhei
authors.initials: Y
authors.lastname: Honda
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Yamada
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Tsutsui
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009543:Nifedipine / Q000494:pharmacology / Q000627:therapeutic use*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D020521:Stroke / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology
chemical_list: D000975:Antioxidants; D009543:Nifedipine