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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 effect of sodium aminalicylate (PAS-Na) on learning and memory and the ultrastructure of hippocampus in sub-acute manganese exposure rats. Methods Male rats were intraperitoneally injected with 15 mg / (kg · d) of manganese dichloride for 5 days a week for 3 weeks. Then PAS-Na100 or 200 mg / kg (L- or H-PAS) is injected subcutaneously daily for 5 consecutive weeks. Morris water maze was used to detect the learning and memory abilities of rats. The ultrastructure of hippocampus CA1 area was observed by transmission electron microscopy. Results In the manganese group, the escape latency at 4 and 5 days was significantly different from that in the normal control group. The measured value in H-PAS group was close to normal group, but the difference was not statistically significant (P> 0.05). In the Mn-Mn group, the trajectories of the perforated rings were scattered. The trajectories of the perforated rings in the H-PAS group were concentrated in the target area of the first quadrant, similar to the control group. The degeneration, apoptosis and expansion of neurons in the hippocampus of the Mn-exposed rats, swelling of the neurons, disorganization of the neurofibrils, disruption of the mitochondrial cristae and broadening of the mitochondrial crest space. PAS-Na treatment of rat hippocampal neuronal morphology atypical, mitochondrial structure recovery close to normal in the H-PAS group was more obvious. Conclusion Under the experimental conditions, PAS-Na may interfere with the damage of manganese induced by hippocampal neurons.