Nimodipine modulates Bcl-2 and Bax mRNA expression after cerebral ischemia.
- Author:
Changqin LIU
1
;
Ruixiang ZHOU
;
Shenggang SUN
Author Information
1. Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
drug effects;
Brain Ischemia;
metabolism;
Calcium Channel Blockers;
pharmacology;
Nimodipine;
pharmacology;
Proto-Oncogene Proteins c-bcl-2;
biosynthesis;
genetics;
RNA, Messenger;
biosynthesis;
genetics;
Rats;
Rats, Wistar;
bcl-2-Associated X Protein;
biosynthesis;
genetics
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2004;24(2):170-172
- CountryChina
- Language:English
-
Abstract:
In order to explore whether the member of Bcl-2 gene family, for example, Bcl-2 and Bax, are induced after cerebral ischemia, and whether expression of genes can be modulated by calcium-antagonist, the rat cerebral ischemic models were made by occluding left middle cerebral artery. The expression of Bcl-2 and Bax mRNA was measured by RT-PCR method. After middle cerebral artery occlusion (MCAO), the expression of both Bcl-2 and Bax mRNA were induced. Level of Bcl-2 mRNA increased steadily and level of Bax mRNA increased gradually at first, reached a peak after 24 h, then decreased slowly. After administration of nimodipine, Bcl-2 mRNA was up-regulated in the hippocampus 6 and 24 h after ischemia, while Bax mRNA was down-regulated 6 and 24 h after ischemia. Focal cerebral ischemia can induce proto-oncogenes to express, which was associated with apoptosis. Calcium-antagonist can up-regulate Bcl-2 mRNA and down-regulate Bax mRNA. The increased ratio of Bcl-2 and Bax mRNA may contribute to the anti-apoptic effect of nimodipine. The study indicates that pharmacological modulation of Bcl-2 family member expression could become a new strategy to manage neuronal damage.
