CAJ | 학술논문

目的：通过研究慢性铝暴露对大鼠海马钙离子稳态及CaMKⅡ和 CREB活性的影响，探讨慢性铝暴露诱导神经损伤可能存在的机制。方法选用60只断乳后雄性Wistar大鼠，分为3组，每组20只；设定其中1组为对照组，用蒸馏水喂养；其他2组为铝暴露组，分别用含有0．2％和0．4％ AlCl3的蒸馏水喂养3个月。 Morris水迷宫测定各组大鼠学习记忆能力；Fura2－／AM测定各组大鼠海马神经细胞自由Ca2＋浓度变化；Western印迹方法检测各组大鼠海马中 CaMKⅡ、Ng和CREB的蛋白表达情况。结果大鼠的学习记忆能力明显降低；与对照组相比，铝暴露各组海马神经细胞中〔Ca2＋〕i 呈剂量依赖性升高；CaMKⅡ和CREB总蛋白表达无显著变化，但p－CaMKⅡ、Ng和 p－CREB蛋白表达显著降低（ P＜0．05）。结论慢性铝暴露损伤大鼠的学习记忆可能与上调Ca2＋及抑制CaMKⅡ和CREB活性相关。
목적：통과연구만성려폭로대대서해마개리자은태급CaMKⅡ화 CREB활성적영향，탐토만성려폭로유도신경손상가능존재적궤제。방법선용60지단유후웅성Wistar대서，분위3조，매조20지；설정기중1조위대조조，용증류수위양；기타2조위려폭로조，분별용함유0．2％화0．4％ AlCl3적증류수위양3개월。 Morris수미궁측정각조대서학습기억능력；Fura2－／AM측정각조대서해마신경세포자유Ca2＋농도변화；Western인적방법검측각조대서해마중 CaMKⅡ、Ng화CREB적단백표체정황。결과대서적학습기억능력명현강저；여대조조상비，려폭로각조해마신경세포중〔Ca2＋〕i 정제량의뢰성승고；CaMKⅡ화CREB총단백표체무현저변화，단p－CaMKⅡ、Ng화 p－CREB단백표체현저강저（ P＜0．05）。결론만성려폭로손상대서적학습기억가능여상조Ca2＋급억제CaMKⅡ화CREB활성상관。
Objective To study the potential mechanism of aluminum-induced memory injury through the research on effect of chro-nic aluminum exposure on calcium homeostasis and activities of CaMKⅡand CREB in hippocampus of rats.Methods 60 weaning rats were divided into 3 groups, which were given distilled water containing 0.2% AlCl3 and 0.4% AlCl3 respectively for 3 months to establish the chronic aluminum exposure model.Morris water maze was used to evaluate the learning and memory ability;the freedom Ca2+in hippocampal neurons of rats was measured with Fura-2/AM;Western blot was used to determine the expressions of CaMKⅡ, Ng and CREB.Results Learning and memory abilities of rats were significantly reduced;the expressions of p-CaMKⅡ, Ng and p-CREB in the hippocampus of alu-minum-treated groups were significantly lower than those in control group(P<0.05), but there were no changes in the expressions of total CaMKⅡand CREB;and the aluminum-treated groups had the higher Ca2+level than that of control group(P<0.05).Conclusions Chronic aluminum exposure could impair the ability of learning and memory of rats, which is closely related to the up-regulation of Ca2+level and the down-regulation of CaMKⅡand CREB activities.