Escitalopram Could Improve The Cognitive Function Of Chronic Cerebral Ischemia Rats

Background and objectiveWith the development of science and technology, the improvement of people’sliving standards, people live longer, the accelerating rhythm of life as well as theenvironmental pollution is aggravating, stroke incidence and morbidity process thetrend of increased year by year.Not only can cause cerebral apoplexy hemiplegia,partial body paresthesia, hemianopsia, aphasia, lack of practical and a series ofnervous system symptoms and signs, still can cause cognitive dysfunction and thepsychological, physiological, social cause depression in patients with all kinds offactors, from the convict, interest in reducing as the main performance of poststrokedepression.PSD is the result of comprehensive shaping of many factors, bothdomestic and abroad, its incidence is generally higher, reported by foreignconcentration between30%-30%, domestic reports is larger, the difference of thedistribution between34.2%-79%. PSD not only affects the recovery of neuralfunction in patients with cerebral apoplexy, also brings to the families of patients withadditional economic and mental burden, therefore the PSD of formal treatment cannot be ignored.5-HT reuptake inhibitors (selective serotonin reuptake inhibitors, SSRIs) canimprove the depressive state of patients with PSD, speed up the restore nerve function,and the less the digestive tract, headache and long QT and other adverse reactions, themost commonly used in clinical for senile patients with PSD, however the drugeffects on cognitive function in patients with cerebral apoplexy opinions vary, soexplore SSRIs effects on cognitive function in patients with chronic cerebral ischemiais extremely important.Chronic cerebral ischemia is a common neurological pathology. Chronic cerebralischemia, cerebral hypoperfusion always in Vascular dementia (VD), Binswangerdisease,cerebral arteriosclerosis, Alzheimer disease and arteriovenous malformationsof the pathological process of various cerebrovascular disease, the incidence of early cognitive impairment as the main performance, could eventually lead to persistent orprogressive cognitive and neural dysfunction.A large number of studies have shownthat serotonin reuptake inhibitors (SSRIs) on excitatory amino acid, oxidative stressand ischemia hypoxia caused by a variety of mechanisms such as brain injury has aprotective effect. Steckler T scholars think2-VO rats learning ability of frontalcortex and hippocampus was associated with a decrease in late-onset of serotonin. Sowe speculate that serotonin reuptake inhibitors may improve cognitive function inpatients with chronic cerebral ischemia.Escitalopram is a potent class of serotoninreuptake inhibitors (SSRI) antidepressants, compared with the similar drugs, higherselectivity for5-HT receptor, work quickly, is widely used in senile depression andprevention and treatment of depression after stroke. Choong Hyun Lee and othershave confirmed30mg/kg of escitalopram post-processing ischemia re-perfusion inrats, the expression of BDNF can promote hippocampal CA1area, and to protect theneurons of hippocampal CA1region induced by ischemic death, for the influence ofcognitive impairment caused by chronic cerebral ischemia research has not beenreported at home and abroad. This experiment uses2VO model rats, used water maze,Western blot and Golgi observing the division of escitalopram on cognitive functionin chronic cerebral ischemia in rats and the influence of the hippocampus BDNFlevels.MethodsRats were randomly divided into sham-operated group、model group(permanentocclusion of bilateral common carotid arteries,2VO)and experimental group(treatedby escitalopram at the dosage of30mg/kg·d).Rats were selected as Study object at1、2、4、8weeks after administration in each group.Cognitive function was evaluated bythe Morris water maze and the expression of BDNF protein was measured usingWestern blotting and dendritic morphology was studied by Golgi staining.Results1．The effects of ESC on cognitive function in chronic cerebral ischemia in rats In the Morris water maze test, the escape latency of model group andexperimental group obviously extended compared to the sham-operated group(P<0.05), while the escape latency in the experimental group shorter than modelgroup(P<0.05)2．The effects of ESC on hippocampus BDNF expression level in the chroniccerebral ischemia rat hippocampusCompared to the sham-operated group,the expression of BDNF in hippocampusof experimental group and experimental group significantly decreased（P<0.05),while that increased significantly in experimental group compared with the modelgroup（P<0.05) by Western blot test.3．The effects of ESC on hippocampus pyramidal cell morphology in chroniccerebral ischemia ratCompared to the sham-operated group, the dendritic length and arborization andthe density of dendritic spines significantly decreased （P<0.05)in the model groupand experimental group in hippocampal CA1,while that increased significantly inexperimental group compared with the model group（P<0.05)by Golgi staining.ConclusionsEscitalopram could significantly delay the progression of cognitive impairmentinduced by chronic cerebral ischemia in rats, the improvement of learning andmemory may be deuced to the increased expression of BDNF.