摘要
目的:探讨三七皂苷Rg1对大鼠局灶性脑缺血再灌注损伤大脑组织中脑源性神经营养因子(brain-de-rived neurotroph ic factor,BDNF)mRNA表达的影响。方法:雄性SD大鼠36只,随机分为脑缺血再灌注模型组、药物治疗组(100 mg/kg)和阳性药物对照组(尼莫地平,1 mg/kg),采用线栓法制作大鼠局灶性脑缺血再灌注损伤模型,各组分别于术后1、3、5天随机取4只大鼠处死后取出脑组织。提取脑组织的总RNA,进行RT-PCR扩增BDNFmRNA特异性片段,构建重组质粒并测序。以倍比稀释后的重组质粒作为阳性标准模板,使用Taqm an探针法对BDNF mRNA进行实时定量PCR检测,分析各组大鼠脑组织中BDNF mRNA的变化。结果:与模型组及阳性对照组相比,三七皂苷Rg1组能明显改善脑缺血的神经缺失症状,并在各时间段均能上调脑缺血再灌注损伤大鼠的脑组织中BDNF mRNA的含量(P<0.05)。结论:三七皂苷Rg1通过上调大鼠脑缺血再灌注损伤时脑组织中BDNF mR-NA的含量,促进脑组织内BDNF蛋白的合成,BDNF与其特异性受体TrkB相结合,产生相应的效应分子而对缺血神经元起保护作用,从而发挥其对脑缺血损伤的治疗作用。
Objective ： To study the effect of notoginsenoside-Rg1 on expression of BDNF mRNA （ brain-derived neurotrophic factor messenger ribonucleic acid） in cerebrum cortex after MCAO/R（ middle cerebral artery occlusion reperfusion）injury in rat by real-time quantitative polymerase chain reaction. Methods： 36 SD male rats were randomly divided into MCAO/R model group, notogisenoside- Rg1 therapy group（100mg/kg） and the positive medicine control group（ nimodipine 1mg/kg）. The MCAO/R model were made by thread-occluded method. The four rats were randomly taken from each groups and were killed to be breaken out brain tissues as specimens after which were treated with medicine in 1,3,5 days. Total RNA was isolated from cerebrum cortex. Specific oligonucleotide primers of BDNF mRNA gene fragments were amplificated by RT-PCR to construct recombinant plasmid and sequence. To dilute recombinant plasmid didploidly and a quantitative standard curve was completed. Taqman fluomgenic quantitative RT-PCR （FQ-PCR） was set up to detect the BDNF mRNA variety of cerebrum cortex. Results： Compared with the model group and the postive control group, notogisenoside-Rg1 treated groups could obviously improve some nervous deficit symptoms in the cerebral ischemia and increase BDNF mRNA amount that in the cerebrum cortex at different period after rat MCAO/R injury. Conclusion： Notoginsenoside-Rg1 can promote to generating internal BDNF protein in brain by up-regulation the expression of BDNF mRNA amount in the cerebrum cortex. BDNF bind in TrkB, which can give rise to protective effects for ischemic neurons by generating corresponding domino effect molecules. Accordingly it can be as a therapy method in cerebral ischemia injury.
出处
《中药材》
CAS
CSCD
北大核心
2007年第3期313-316,共4页
Journal of Chinese Medicinal Materials
基金
云南省自然科学基金项目(No.2002C0051m)
