| Chronic hypoperfusion, the regional brain injury including the loss of learning and memory function, movement disorders and other symptoms, is caused by the lack of cerebral blood flow perfusion for a long time. This disease has become the second most common type of dementia after the Alzheimer’s disease; therefore, it has important medical value and social significance to control the occurrence of cerebrovascular disease, slowing down disease progression to improve the quality of patients’life. This study mainly investigates protective effects of Tongsaimai tablets on cerebral damage in rats induced by ligation of bilateral common carotid artery and its mechanism. First, rats with bilateral common carotid artery ligation were performed, then randomly dividing into sham group, vehicle group and treatment group. The treatment group, in accordance with the treatment time, is divided into two weeks group and four weeks group, while rats in vehicle group were administrated with the same volume normal saline as in the Tongsaimai treatment group. Then, the Morris water maze experiment was conducted in experimental subjects before and after the drug administration. Results showed that rats with chronic hypoperfusion were having longer latent time, longer swimming distance and shorter platform quadrant. Furthermore, the numbers of neuron in hippocampal cortex cells were markedly decreased in the vehicle group compared to sham group and the brain water content was increased. However, Tongsaimai treatment improved the ability of the learning and memory, inhibited the neuron loss. Our immunohistochemical results found that the astrocytes were remarkably activated in cortex. In addition, ELISA showed that pro-inflammatory factors level of IL-6 in vehicle rats were higher than that of in control group and treatment group. After treatment with Tongsaimai tables, the content of IL-6 gradually declined, and the concentration of cerebral NO in vehicle group and the general expression of iNOS were significantly higher than those of that in control group and treatment group. The Tongsaimai treatment could significantly inhibit astrocyte proliferation, the secretion of EL-6, general NO production, and the expression of iNOS. Moreover, Tongsaimai therapy had a certain inhibitory effect for the expression of caspase-3 caused by chronic hypoperfusion. Importantly, the expression of HO-1 in the treatment group was significantly increased. The above results suggest that Tongsaimai tablets may exert the protective effects on chronic hypoperfusion-induced injury via up-regulating the expression of HO-1, inhibiting the excessive inflammatory response and apoptosis. |