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机构地区:[1]吉林大学白求恩第一医院神经内科,吉林长春130021
出 处:《中风与神经疾病杂志》2012年第9期776-779,共4页Journal of Apoplexy and Nervous Diseases
基 金:吉林省卫生厅科研项目(编号:20082028)
摘 要:目的检测慢性酒精中毒大鼠脑组织钙神经素(calcineurin,CaN)的异常分布与表达及离子变化情况,探讨慢性酒精中毒代谢性脑病的发病机制。方法选用健康雄性Wistar大鼠100只,随机分为2组,酒精中毒组60只,盐水对照组40只。正常喂养1w后开始造模。酒精中毒组(60只):每日每只大鼠分别按8ml/kg灌胃2w,随后再按照10ml/kg灌胃1w,按12ml/kg灌胃1w,共灌胃4w。每日灌胃2次,其间隔均为6h,酒精浓度为50%。盐水对照组(40只):同时用等量的生理盐水进行灌胃。每周测量体重,观察其一般生物学特征;免疫组化法测定CaN的阳性表达;原子吸收法测定Ca2+、Mg2+、K+、Na+等微量元素变化。结果两组大鼠一般生物学特征存在明显差异,体重差异具有的统计学意义;酒精组大鼠大脑皮质、海马CaN表达明显多于对照组(P<0.05),小脑CaN表达无差异(P>0.1);原子吸收法测定酒精组的Ca2+含量比正常对照组明显增多(P<0.05),Mg2+、K+、Na+含量无显著变化(P>0.05)。结论慢性酒精中毒后可以引起大鼠大脑皮质、海马CaN异常表达及Ca2+含量明显增多,推测酒精中毒后可对神经元产生以Ca2+代谢为主的影响,导致酒精中毒性代谢性脑病的发生。Objective To investigate expression and change of CaN and ion in cerebral cortex,hippocampus and cerebellum of alcoholism rats,and to discuss pathogenesis of alcoholic metabolic encephalopathy.Methods There were healthy 100 male Wistar rats divided into 2 groups randomly.Alcoholism group had 60 rats and saline control group,40.The model was performed a week after normal feeding.In alcoholic group,every rat was fed with 50% alcohol(8ml/kg)twice a day;two weeks later,10ml/kg;a week later,12ml/kg,and the intervals of time were 6 hours of all.In control group,every rat was fed with the same dosage of 0.9% sodium chloride at the same time,the total time of this test was four weeks.During the experiment,we measured their weight periodically,determined the positive expression of CaN by SP dying method,observed the two group of rats with their general condition,determines the change of Ca2+,K+,Mg2+,Na+ and so on trace element with atomic absorption method.Results After 4 weeks,the alcoholic group rats appeared malnutrition,emaciated,moreover some also appeared the performance which the nervous system damages.Alcoholic groups increased CaN expression by SP dying method in cerebral cortex and hippocampus of alcoholism rats(P0.05),while there were no difference in cerebellum(P0.1).The alcoholic group's Ca2+ content increased obviously compared to the normal control group,while Mg2+,K+ and Na+ content was not remarkable changed(P0.05).Conclusion Chronic alcoholism may cause CaN masculine to express in rats cerebral cortex and the hippocampus,and the Ca2+ content to increase,and they may participate the occurrence and development of metabolic encephalopathy.
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