Purpose: Chronic cerebral ischemia is a common pathological state, which can lead to cognitive disorder and neurological dysfunction. Aminoguanidine is a selective iNOS inhibitor which can improve acute cerebral ischemia, however its protective effect against chronic ischemic neurological damage remains to be researched. This study analyses the effect of aminoguanidine intervention on hippocampal pyramidal cell dendrite morphological change and spinophilin expression of rats with chronic cerebral ischemia, so as to explore its cerebral protection mechanism.
Method: Prepare chronic cerebral ischemia model, conduct aminoguanidine lavage intervention, and then evaluate behaviors of each group of rats through Morris water maze at the 2nd, 4th, 8th week, respectively. Conduct Golgi stain, and observe branching and length change of hippocampal pyramidal cell dendrite; conduct immunohistochemical method to test spinophilin expression of each group of rats.
Results: SD rats were randomly divided into sham-operated group, model group (2VO group), and intervention group (aminoguanidine group). Compared with sham-operated group, the branches and length of hippocampal pyramidal cell dendrite of rats in model group at the 4th and 8th week were significantly reduced (P<0.05), and the spinophilin expression of model group was significantly reduced (P<0.05), showing a progressive behavioral and cognitive dysfunction; Compared with model group, the dendrite branches and length, and spinophilin expression of intervention group were significantly increased (P<0.05).
Conclusion: Aminoguanidine can promote hippocampal pyramidal cell dendrite morphological change and increase spinophilin expression of rats with chronic cerebral ischemia. Through such approach, it can improve chronic cerebral ischemia anoxic condition and the damage process of hippocampal pyramidal dendrite and dendrite spine, maintain normal transmission of synapse, so as to exert brain protection effect and improve cognitive disorder caused by chronic cerebral ischemia.