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.
出处
《中国卫生产业》
2014年第11期20-20,22,共2页
China Health Industry
关键词
铝中毒
海马CA3区
突触体素
大鼠
Aluminum Toxicosi
Synaptophysin
Hippocampal CA3 area
Rats