高胆固醇血症促进淀粉样蛋白在铝中毒小鼠脑内沉积  

Hypercholesterolemia accelerates the amyloid pathology in model mice induced by aluminum intoxication

作　　者：李恒华[1] 孙峰[1] 刘颖菊[1] 高丽佳[1] 

机构地区：[1]重庆医科大学药理教研室,重庆400016

出　　处：《重庆医科大学学报》2007年第6期619-622,共4页Journal of Chongqing Medical University

摘　　要：目的:观察高胆固醇血症对铝中毒致小鼠神经元损伤的促进作用。方法:小鼠给予铝400mg(/kg.d)连续灌胃10周,实验第3周起改饲高胆固醇饮食至第10周末。结果:铝中毒组和铝中毒联合高胆固醇饮食组小鼠空间识别能力明显减退(P<0.05),海马CA1、CA2区神经元明显损伤。与单纯铝中毒组相比,铝中毒联合高胆固醇饮食组血清总胆固醇明显升高(P<0.05),小鼠空间识别能力下降程度和海马神经元损伤更明显,刚果红染色显示海马神经元损伤区出现淀粉样蛋白沉淀。结论:高胆固醇血症能加重铝中毒导致的神经元损伤,其机制可能跟促进淀粉样蛋白沉积有关。Objective：To investigate the aggravating effects of hypercholesterolemia on the damage to neurons induced by aluminum intoxication in mice. Methods：Aluminum was given by gavage with A1 400 mg/ （kg·d） for 10 weeks. Mice were placed on high-cholesterol diet the third week after A1 was given. Results：The spatial recognition ability decreased significantly（P〈0. 05） and hippocampal neurons （CA1,CA2）were damaged obviously in mice with aluminum and with or without high-cholesterol diet, compared with control group with basal diet. Moreover, the impairment of spatial recognition ability and the damage to neurons were more serious and pathological changes of amyloid in the bippocampus （CA1 ,CA2）with CR staining were found in mice with aluminum and high-cholesterol diet. Conclusions：Hypercholesterolemia may aggravate the damage to neurons induced by aluminum intoxication and its mechanisms might involve the acceleration of the amyloid deposition.

关 键 词：高胆固醇血症 淀粉样蛋白 铝 

分 类 号：R749[医药卫生—神经病学与精神病学]