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机构地区:[1]黔西南州人民医院神经内科,贵州兴义562400 [2]贵阳医学院解剖学教研室,贵州贵阳550004
出 处:《中国卫生产业》2014年第11期20-20,22,共2页China Health Industry
摘 要:目的通过突触体素(Synaptophysin,p38)的表达,探讨铝的神经毒性作用机理。方法40只4~5月龄sD大鼠,随机分为两组:铝中毒组和正常对照组,每组20只,雌雄各半。常规p38免疫组化染色,用细胞形态学计量方法测量p38阳性产物的平均光密度。结果铝中毒组大鼠海马CA3区神经元p38免疫组化染色阳性颗粒减少,阳性产物平均光密度降低,与正常对照组比较,差异有统计学意义(P〈0.01)。结论慢性铝中毒引起大鼠海马CA3区p38的减少。这种变化可能是铝的神经毒性作用机理之一。Objective To study the p38-positive outgrowth change of the hippocampal CA3 area of rats with chronic aluminium toxicosis.Methods 40 Sprague-Dawley rats of 4 -5 months age were randomly divided into two groups:The aluminum exposed group, aluminum were gaved for 3 months by digestive tract ( 100mgAlcl3/kg/d),and normal control group, only equal distilled water were gaved, the p38-positive outgrowth in the hippocampal CA3 area were quantitatively analyzed with cell morphometric technique. Results The average optical density of p38 immunoreactivity positive structure were significantly decreased too in alu- minum exposed group than in the normal control group. Conclusion Aluminum can decrease the synthesis of p38 in the hip- pocampal CA3 area.It might be one of the mechanisms of aluminum neurotoxicity.
分 类 号:R322.81[医药卫生—人体解剖和组织胚胎学]
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