Neutroprotective efficacy of sodium tanshinone B on hippocampus neuron in a rat model of focal cerebral ischemia

• DOI: 10.1007/s11655-012-1266-9
• Publication Date: 2012-10-19T02:22:29Z
• Authors: Qing Cai; Hong-wu Wang; Sheng-yu Hua; Jun-zhen Tan; Tao Zhou; Chun-shen Li
• Keywords: Neurons; 0301 basic medicine; Drug Evaluation, Preclinical; Hippocampus; Models, Biological; Brain Ischemia; Rats; 3. Good health; Disease Models, Animal; Random Allocation; 03 medical and health sciences; Neuroprotective Agents; Treatment Outcome; 0302 clinical medicine; Cytoprotection; Reperfusion Injury; Abietanes; Animals; Drugs, Chinese Herbal

To investigate the protective effects of sodium tanshinone B (STB) on brain damage following focal ischemia-reperfusion (I/R) injury through interfering with N-methyl-D-aspartic acid receptor (NMDAR) and excitatory and inhibitory amino acids, and evaluate the potential mechanisms of the neuroprotective activity of STB.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 (STB(1), STB(2), STB(3)) for 3 days before MCAO. The expression of NMDAR1 was detected by immunohistochemistry and Western blotting. The concentrations of glutamate and γ-aminobutyric acid (GABA) were analyzed using high performance liquid chromatography.STB treatment reduced neurological defect scores, cerebral infarction volume and brain water content. The levels of NMDAR1 were significantly higher in the l/R and STB(1) groups than that of the sham and the STB(3) groups (P<0.01). Optical density of NMDAR1 was significantly increased in cornu ammonis (CA)1 region of the l/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 STB(3) group than that of the l/R, STB(1) and STB(2) groups (P<0.01).Preconditioning with STB appears to be a simple and promising strategy to reduce or even prevent cerebral l/R injury and has potential for future clinical application.