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目的通过对鱼藤酮导致慢性中毒SD大鼠脑组织标本的病理学检测,探讨鱼藤酮损伤脑神经元的作用机制。方法将20只雄性SD大鼠随机分为两组,实验组:1.5 mg/(kg·d)的鱼藤酮颈背部皮下注射8周,共10只;对照组:相同体积的葵花油颈背部皮下注射8周,共10只。实验中观察各组大鼠的一般情况并每周进行行为学测试及体重的测量。选取实验组全部存活的SD大鼠脑组织标本,共6个;在对照组中随机选取6个脑组织标本。随后进行HE染色,并用显微镜观察组织的病理变化。结果实验结束时,实验组大鼠共死亡4只,对照组无死亡现象。实验组大鼠在实验中表现出较为明显的毛色泛黄、反应迟钝、精神萎靡、活动减少、进食缓慢等中毒症状。在体重增长速度上与对照组比较,差异有统计学意义(P<0.05)。在行为学上,实验组大鼠在网格实验中表现出了较为明显的行为学异常,第7、8周时两组大鼠移动的潜伏时间比较,差异有统计学意义(P<0.05)。大鼠脑病理学检测提示实验组大鼠脑干区可见神经元数目减少、核固缩、变性等改变。黑质致密部多巴胺(dopanine,DA)神经元变性。对照组大鼠未见明显异常。结论鱼藤酮导致慢性中毒的SD大鼠脑组织神经元发生损伤,并出现神经系统相关的行为学表现,推测鱼藤酮造成线粒体损伤是导致神经元变性坏死的主要原因。
OBJECTIVE: To investigate the pathological mechanism of rotenone-induced neuronal injury in brain of rats with chronic poisoning induced by rotenone. Methods Twenty male Sprague-Dawley rats were randomly divided into two groups. In the experimental group, 10 rabbits were injected subcutaneously with 1.5 mg / (kg · d) of rotenone on the back of the neck for 10 weeks. The control group: 8 weeks, a total of 10. In the experiment, the general situation of rats in each group was observed and behavioral tests and weight measurements were performed weekly. A total of 6 SD rats brain tissue samples were selected for experiment group survival, and six brain tissue samples were randomly selected from the control group. Subsequently, HE staining was performed and the histopathological changes of the tissues were observed with a microscope. Results At the end of the experiment, 4 rats died in the experimental group and no death occurred in the control group. Experimental rats in the experiment showed more obvious yellow hair color, unresponsive, apathetic, activity decreased, eating slowly and other symptoms of poisoning. Compared with the control group, there was a significant difference in the rate of weight gain (P <0.05). In behavioral science, experimental rats showed obvious behavioral abnormalities in grid experiment. There was significant difference in the latency of movement between the two groups at the 7th and the 8th week (P <0.05) . The pathological examination of rat brain showed that the number of neurons in the brainstem area of the experimental group was decreased, and nuclear condensation and degeneration were observed. Dopaminergic dopamine (DA) neuronal degeneration. The control group rats showed no obvious abnormalities. Conclusion Rotenone causes neuronal damage in the brain of SD rats with chronic poisoning and neurological related behavioral findings. Speculated that rotenone causes mitochondrial damage is the main reason leading to degeneration and necrosis of neurons.