OBJECTIVE: To study the effect of notoginsenoside-Rg, 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 (100 mg/kg) and the positive medicine control group (nimodipine 1 mg/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 fluorogenic 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.
OBJECTIVE: To study the effect of notoginsenoside-Rg, 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 (100 mg/kg) and the positive medicine control group (nimodipine 1 mg/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 fluorogenic 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 ratMCAO/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.