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作 者:谢武桃[1] 贺进[1] 李庆春[1] 邹聪[1] 徐晨[1]
机构地区:[1]重庆医科大学基础医学院电镜室,重庆400016
出 处:《重庆医科大学学报》2010年第1期25-28,共4页Journal of Chongqing Medical University
基 金:重庆市高等学校优秀人才资助计划项目[渝教人(2009)2号]
摘 要:目的:探讨小剂量慢性镉中毒法建立大鼠肌萎缩侧索硬化症动物模型的可行性。方法:成年大鼠饮水慢性染镉,每天饮用含镉去离子水(150mg/L),记录每天饮水量,120d后取材。采用神经电生理、光镜、电镜技术测定大鼠坐骨神经传导速度、股二头肌形态学变化、脊髓前角运动神经元形态学变化;同时采用原子吸收石墨炉法、生物化学技术测定脊髓内镉含量以及脊髓组织细胞内铜锌超氧化物歧化酶1(CuZn-SOD1)活性、丙二醛含量的变化。结果:染镉后120d,大鼠运动神经传导速度减慢但股二头肌纤维直径变化不明显;脊髓前角运动神经元胞体平均截面积有变小、神经元胞浆内粗面内质网排列紊乱并出现核糖体脱颗粒现象;染镉后脊髓内镉含量增加、脊髓组织匀浆内CuZn-SOD1酶活性降低,而丙二醛含量升高。结论:镉可以在成年大鼠脊髓内蓄积,导致前角运动神经元形态和功能损伤。提示慢性镉中毒法可用于建立大鼠肌萎缩侧索硬化症的动物模型。Objective: To study the feasibility of making animal model of amyotrophic lateral sclerosis using low dose chronic cadmium poisoning method in rats. Methods:Aduh SD rats were treated with cadmium chloride (150mg/L) by drinking for 120 days. Motor nerve conduction velocity, the morphologieal changes of musculus biceps femoris and spinal motor neuron were studied with electrophysiolog-ical technique,light and electron microscopy. The content of cadmium in the spinal cord,the active change of CuZn-SOD~ and MDA were measured with the atomic absorption and biochemistry techniques. Results: 120 days after the cadmium ( Cd ) treatment in rats, the motor nerve conduction velocity were slow down in the Cd group. However, no obvious change was found in the muscle fiber diameter between Cd and control group. The mean cross-sectional areas of spinal motorneurons were decreased and the degranulation of ribosomes were found in some motorneurons. The content of Cd in spinal cord increased significantly after Cd exposure. The enzymatic activity of CuZn-SOD1 was weak and the content of MDA increased in Cd group. Conclusion: Chronic low dose Cd exposure can deposit in the spinal cord of adult rats. It may cause functional change in spinal motorneurons and motor nerve fibers, which can be the method to make the animal model of amyotrophic lateral sclerosis.
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