摘要
AIM:In order to explore whether the member of Bcl-2 gene family,for example,B cl-2 and Bax,are induced after cerebral ischemia,and whether expression of gene s can be modulated by calcium-antagonist.METHODS:The rat cerebral ischemic mode ls were made by Nagasawa and Zea Longa improvement method,by occluding left midd le cerebral artery;the expression of Bcl-2 and Bax mRNA were measured by RT-PC R method.RESULTS:After administration of nimodipine, Bcl-2 mRNA was up-regulat ed in the hippocampus at 6 and 24 h after ischemia,while Bax mRNA was down-regu lated at 6 and 24h after ischemia.CONCLUSION:Calcium-antagonist can up-regulat e Bcl-2 mRNA and down-regulate Bax mRNA.Increasing the ratio of Bcl-2 and Bax mRNA may contribute to the anti-apoptic effect of nimodipine.
AIM:In order to explore whether the member of Bcl-2 gene family,for example,B cl-2 and Bax,are induced after cerebral ischemia,and whether expression of gene s can be modulated by calcium-antagonist.METHODS:The rat cerebral ischemic mode ls were made by Nagasawa and Zea Longa improvement method,by occluding left midd le cerebral artery;the expression of Bcl-2 and Bax mRNA were measured by RT-PC R method.RESULTS:After administration of nimodipine, Bcl-2 mRNA was up-regulat ed in the hippocampus at 6 and 24 h after ischemia,while Bax mRNA was down-regu lated at 6 and 24h after ischemia.CONCLUSION:Calcium-antagonist can up-regulat e Bcl-2 mRNA and down-regulate Bax mRNA.Increasing the ratio of Bcl-2 and Bax mRNA may contribute to the anti-apoptic effect of nimodipine.
出处
《中国临床康复》
CSCD
2003年第4期672-673,共2页
Chinese Journal of Clinical Rehabilitation
关键词
钙拮抗剂
缺血性脑损伤
BCL-2
Bax
基因表达
calcium channel blockers
brain ischemia/genetics
gene expression regulation
genes
