Abstract

Patients with vascular dementia are unable to live freely due to diminished cognitive function and daily life skills. It is vital to identify new medical therapies since, at the moment, anti-dementia medications only temporarily alleviate patients’ clinical symptoms and have no impact on slowing the progression of the disease or enhancing the prognosis of the condition. In this work, a permanent bilateral common carotid artery blockage was used to create a rat model of vascular dementia. The rats that were effective at modeling were divided into four groups namely, model, high-dose Tong Qiao Yizhi granules group, medium-dose Tong Qiao Yizhi granules and memantine group. After 30 d of intragastric injection, the behavioral alterations in the rats in each group were noted. By using golgi staining, the density of dendritic spines was discovered. Further, hippocampus cornu ammonis 1 region’s synapses’ was examined using transmission electron microscopy. By using an immunofluorescence test, the glutamate receptor subunits expression levels in the hippocampus cornu ammonis 1 area were discovered. The expression of synaptic growth associated protein-43, synaptophysin and postsynaptic density protein 95; expression of important pathway components like mitogen activated protein kinase enzymes 1/2, phospho-mitogen activated protein kinase enzymes, extracellular signal-regulated protein kinases 1/2, phospho-extracellular signal-regulated protein kinase and cyclic adenosine monophosphate response element binding protein/phospho-cyclic adenosine monophosphate response element binding protein were all detected in the hippocampus through Western blotting. The findings demonstrated that Tong Qiao Yizhi granules might enhance cognitive function and synaptic ultrastructure in the hippocampus cornu ammonis 1 area among the vascular dementia rats, as well as greatly increase the density of dendritic spines. We deduced that Tong Qiao Yizi granules can significantly enhance the learning and memory capacity of vascular dementia rats based on the aforementioned findings. The process may involve activating cyclic adenosine monophosphate response element binding protein to increase synaptic plasticity and upregulate the phosphorylation levels of mitogen activated protein kinase enzymes 1/2 and extracellular signal-regulated protein kinases 1/2 and important components of the mitogen activated protein kinases/extracellular signal-regulated kinase signaling pathway, in order to improve the memory impairment in vascular dementia rats.