| ObjectCognition dysfunction is major clinical manifestation of Central nervous system complication due to chronic intermittent hypoxia, more and more attention has been paid to the relationship between cognition dysfunction and OSAHS for the past years .nevertheless ,specific mechanisis still indefinite. Apoptosis played important role in various CNS disease, but rare report with the central nervous system affection of OSAHS. likewise; research has indicated that IGF-1 protein may be of close association with cognition dysfunction. In this research, experiments were carried out on the influence about cognition in OSAHS rats, the number of apoptosis neuron in hippocampus ,the expression of IGF-1 protein in CA1 region of hippocampus; so that we look forward to investigate the possible association between them and their possible effect in cognition dysfunction of CIH, So it will supply with essential laboratory evidences for the clinical therapy and prevention of cognition dysfunction of CIH.Methods1. Establishment of chronic-intermittent hypoxia model in rat: Sixteen three-month old male Sprague-Dawley rats were chosen. The sixteen rats were randomly assigned to two experimental groups (n = 8/group): chronic intermittent hypoxia group(CIH) ,unhandled control group (UC).Animals from UC group were raised under physiological conditions, animals in CIH group were kept in the plexiglass chamber between 9Am-5Pm and underwent intermittent hypoxic challenge (oxygen concentration ranged from lowest 8.5%—21%, 8 minutes of each cycle) for 8h/day for 4weeks. Room temperature was 25±1°C,The feedstuff and water were same for all rats . Pressure, temperature and humidity inside the plexiglass chamber were standardized. The duration of experiment was 8 weeks.2.The determination of the ability of lerning and memory: The ability of learning was evaluated according to mean escape latency. The ability of memory was evaluated according toui the number of times of crossing the platform and the percentage of time spending on the target quadrant to the total swimming time.3.The determination of morphology and serology: The rats were routinely sacrificed at the end of experiment, the changes of the following indexes were observed : the general pathological changes(HE staining) and the ultrastructure of brain ; the number of apoptosis neuron in hippocampus(TUNEL);the expression of IGF-1 protein in CA1 region of hippocampus ( immunohistochemistry staining,SP stain);Results1. Morris water maze test Learning scores(position navigation):After 5 days training, the escape latency in CIH rats was significantly longer compared with that in UC rats (p<0.05);2. .Morris water maze test memory scores:The number of times of crossing the platform in CIH group [(1.38±0.92)] was significantly reduced compared with that in UC group [(3.75±1.04), p <0.01];The percentage of time spent on crossing the target quadrant to the total swimming time in CIH group (20.52±3.41) was also significantly decreased compared with that in UC group [(39.89±5.63), P<0.01];2. (1)Changes in the ultrastructure of hippocampus neurons and synapsis were obvious in chronic intermittent hypoxia group as compared with the unhandled control group;(2) the number of TUNEL positive neuron in CA1 region of hippocampus increased ,AI is obviously higher than UC, the difference between the two groups is statistically significant(P<0.05); (3)The expression of insuline-like growth factor-1 in CA1 region of hippocampus in CIH was obviously decreased compared with that in UC group (p < 0.05, There was negative correlation between cognition impairment in rats and the expression of IGF-1 in CA1 region of hippocampus(r=0.867, p <0.01);Conclusion1. Chronic intermittent hypoxia can lead to cognitive impairment of the rats 2. The neuron apoptosis in CA1 region of hippocampus and the expression of Insulin-like growth factor-1 decreased may be one of mechanism that chronic intermittent hypoxia lead to cognitive impairment of the rats... |
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