摘要
Objective： To investigate the protective effects of sodium tanshinone B （STB） on brain damage following focal ischemiareperfusion （I/R） injury through interfering with NmethyIDaspartic acid receptor （NMDAR） and excitatory and inhibitory amino acids, and evaluate the potential mechanisms of the neuroprotective activity of STB. Methods： Transient forebrain ischemia was induced by middle cerebral artery occlusion （MCAO）. The rats were randomized into a sham operated group, a model group （I/R） and three STB different dose groups. Rats were pretreated with STB at the doses of 4, 8, 16 mg/kg （STB1, STB2, STB3） for 3 days before MCAO. The expression of NMDAR1 was detected by immunohistochemistry and Western blotting. The concentrations of glutamate and λaminobutyric acid （GABA） were analyzed using high performance liquid chromatography. Results： STB treatment reduced neurological defect scores, cerebral infarction volume and brain water content. The levels of NMDAR1 were significantly higher in the I/R and STB1 groups than that of the sham and the STBs groups （P〈0.01）. Optical density of NMDAR1 was significantly increased in cornu ammonis （CA）I region of the I/R group （P〈0.05）. STB treatment reduced NMDAR1 optical density in the CA1 region （P〈0.01）. The levels of glutamate were significantly lower in the hippocampus in the STB3 group than that of the I/R, STB1 and STB2 groups （P〈0.01）. Conclusion： Preconditioning with STB appears to be a simple and promising strategy to reduce or even prevent cerebral I/R injury and has potential for future clinical application.
Objective： To investigate the protective effects of sodium tanshinone B （STB） on brain damage following focal ischemiareperfusion （I/R） injury through interfering with NmethyIDaspartic acid receptor （NMDAR） and excitatory and inhibitory amino acids, and evaluate the potential mechanisms of the neuroprotective activity of STB. Methods： Transient forebrain ischemia was induced by middle cerebral artery occlusion （MCAO）. The rats were randomized into a sham operated group, a model group （I/R） and three STB different dose groups. Rats were pretreated with STB at the doses of 4, 8, 16 mg/kg （STB1, STB2, STB3） for 3 days before MCAO. The expression of NMDAR1 was detected by immunohistochemistry and Western blotting. The concentrations of glutamate and λaminobutyric acid （GABA） were analyzed using high performance liquid chromatography. Results： STB treatment reduced neurological defect scores, cerebral infarction volume and brain water content. The levels of NMDAR1 were significantly higher in the I/R and STB1 groups than that of the sham and the STBs groups （P〈0.01）. Optical density of NMDAR1 was significantly increased in cornu ammonis （CA）I region of the I/R group （P〈0.05）. STB treatment reduced NMDAR1 optical density in the CA1 region （P〈0.01）. The levels of glutamate were significantly lower in the hippocampus in the STB3 group than that of the I/R, STB1 and STB2 groups （P〈0.01）. Conclusion： Preconditioning with STB appears to be a simple and promising strategy to reduce or even prevent cerebral I/R injury and has potential for future clinical application.
基金
Supported by Science Development Foundation of Tianjin Institute of Education(No.20070301)
Tianjin Natural Science Foundation of China(No.11JCYBJC13400)
