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目的研究鱼藤酮对大鼠脑黑质多巴胺能神经体系及氧化应激参数(丙二醛和谷胱甘肽)的影响,探讨鱼藤酮对多巴胺能神经元的毒性作用及其发病机制。方法实验组10只大鼠背部皮下注射鱼藤酮1.0 mg/(kg·d),对照组10只大鼠背部皮下注射葵花籽油1 m L/kg,两组均注射50 d。以免疫细胞化学技术检测大鼠脑内酪氨酸羟化酶(TH)的表达改变,并采用分光光度法检测大鼠脑内氧化应激参数(丙二醛和谷胱甘肽)的改变。结果大鼠多巴胺能神经元有不同程度的损伤,大鼠脑内TH免疫反应强度在黑质和纹状体都有明显的降低,实验组黑质TH免疫反应阳性神经元数目明显少于对照组(P<0.01);分光光度计法检测中脑黑质中谷胱甘肽,在实验组中较对照组明显减低,差异有统计学意义(P<0.01),丙二醛在实验组中较对照组明显增高,差异有统计学意义(P<0.01)。结论鱼藤酮具有明显的神经毒性,能导致大鼠脑内多巴胺能神经元的损伤,导致大鼠脑内发生明显氧化应激损伤。
AIM To investigate the effects of rotenone on dopaminergic neurons and oxidative stress parameters (MDA and GSH) in the substantia nigra of rats and to explore the toxic effects of rotenone on dopaminergic neurons and its pathogenesis. Methods Ten rats in the experimental group were injected subcutaneously with 1.0 mg / (kg · d) rotenone on their backs. Ten rats in the control group were subcutaneously injected with 1 m L / kg of sunflower seed oil on their backs for 50 days. The changes of tyrosine hydroxylase (TH) expression in rat brain were detected by immunocytochemistry, and the changes of oxidative stress parameters (malondialdehyde and glutathione) in rat brain were detected by spectrophotometry. Results Rat dopaminergic neurons were damaged to some extent. The intensity of TH immunoreactivity in rat brain was significantly reduced in substantia nigra and striatum. The number of TH immunoreactive neurons in substantia nigra was significantly less in experimental group than in control group (P <0.01). Glutathione (GSH) in the midbrain substantia nigra was significantly decreased by spectrophotometry in the experimental group compared with the control group (P <0.01). Compared with the control group Group was significantly higher, the difference was statistically significant (P <0.01). Conclusion Rotenone has obvious neurotoxicity, which can lead to the damage of dopaminergic neurons in rat brain, leading to obvious oxidative stress injury in rat brain.