Objective:To discuss the influence of prescription-Tongmai Yizhi (TMYZ) on the behavior, histology and Cyclin-dependent kinase-5(Cdk5) expression level in Alzheimer’s disease(AD) model rat; to explore the potential key intervention link of TMYZ on the AD pathological process.Methods:To build AD model rats by injecting10μg/4μL mixture of aggregated A β1-10and IBO to the left hippocampal CA1areas of SD rats; to observe the effect of TMYZ on the learning and memory in AD model rats through hidden-platform acquisition test of the SLY-WMS morris water maze; to observe the protective effect of TMYZ on the neuron in hippocampus in AD model rats by reading HE staining sections under the computer-assisted light microscope; to detect the influence of TMYZ on the expression level of Cdk5protein and gene by Western Blotting and Real-time quantitative PCR.Results:The water maze test revealed that TMYZ significantly enhanced the cognitive ability and memory of AD model rats. HE staining sections also illustrated that TMYZ attenuated the hippocampal neuron injury in AD model rats including hippocampal neuronal swollen, neuronal-vacuolar degeneration, nucleus shrinkage or disappearance and disorganized pyramidal neuron. This study also indicated that TMYZ could decrease the expression level of Cdk5protein and gene detected by Western Blotting and Real-time quantitative PCR.Conclusion:TMYZ might play the neuroprotective effects by decreasing the expression level of Cdk5protein and gene to keep Cdk5activity within a proper level. Further, proper Cdk5activity level could inhibit generation of Aβ and hyperphosphorylation of Tau. We may get a conclusion that Cdk5might be the key protein kinase during the intervention of TMYZ on the AD pathological process. |