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作 者:邓祥发[1,2] 陈海滨[1] 姜岳明[1] 罗海兰[1] 区仕燕[1] 陆继培[1] 邓欣[1] 卢珊[1] 王坤[1] 蒋艺华[1] 李罡[1]
机构地区:[1]广西医科大学公共卫生学院卫生毒理学教研室,广西南宁530021 [2]广西医科大学基础医学院人体解剖学教研室
出 处:《毒理学杂志》2010年第1期5-9,共5页Journal of Toxicology
基 金:国家自然科学基金项目(30760210);广西教育厅研究生教育创新计划(2008105981004D32)
摘 要:目的研究对氨基水杨酸钠(PAS-Na)对亚急性锰暴露大鼠学习记忆及海马超微结构改变的影响。方法雄性大鼠腹腔注射(ip)二氯化锰15mg/(kg·d),每周5天,连续3周。然后每日背部皮下注射PAS-Na100或200mg/kg(L-或H-PAS),连续5周。采用Morris水迷宫检测大鼠学习记忆能力,透射电镜观察大鼠海马CA1区超微结构变化。结果染锰组第4和5天逃避潜伏期、游泳总路程与正常对照组差异较大;H-PAS组测得值接近正常组,但是差异无统计学意义(P﹥0.05)。染锰组穿环轨迹路线比较分散,H-PAS组穿环轨迹路线集中于第一象限目标区,与对照组相似。染锰大鼠海马神经元出现变性、凋亡和胀亡,神经元突起肿胀,神经原纤维排列紊乱、中断,线粒体嵴间隙增宽,崩解呈空泡状。PAS-Na治疗后大鼠海马胀亡神经元形态不典型,线粒体结构恢复接近正常,在H-PAS组较为明显。结论在本试验条件下,PAS-Na对锰致海马神经元的损害可能有干预作用。Objective To study the effects of sodium para-aminosalicylic acid on learning,memory and hippocampal ultramicro-structure of subacute manganese-exposed rats.Methods Male rats were intraperitoneally given manganese chloride(15 mg/kg) daily for 3 weeks(5 days/week).And then,rats were treated on 35 days with PAS-Na at 100 or 200 mg·kg-1 by subcutaneous injection in the back.The ability of learning and memory was tested by Morris Water Maze(MWM) and the alterations of ultramicro-structure in hippocampal CAI area of rats were observed by transmission electron microscope.Results The escaping latency and swimming distance of manganese-exposed group were different from the control group in the 4 th and 5 th day.The scores of treated group with PAS-Na at 200 mg/kg(H-PAS) were close to the control group,which was not significantly(P ﹥ 0.05).In spatial probe test,track routers of perforating in H-PAS group were located in target zone of the 1 st quadrant that was close to the control group,which was different from the manganese-exposed group.The pathological changes of hippocampal ultramicro-structure,such as the degeneration,apoptosis and oncosis in neurons,swelling in neuronal process,derangement and interruption in neurofibril,broadening,disintegrating and vacuole in ridge gap of mitochondria,were observed in the manganese-exposed rats.Atypical morphology of oncosis in hippocampal neurons was scarcely seen and the recovered mitochondrial structure was close to normal after PAS-Na treatment,particularly common in the H-PAS group.Conclusion PAS-Na may be an antagonism on the injured neurons in hippocampus of the manganese-exposed rats.
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