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首页> 外文期刊>Neurotoxicity research >Nifedipine prevents iron accumulation and reverses iron-overload-induced dopamine neuron degeneration in the substantia nigra of rats
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Nifedipine prevents iron accumulation and reverses iron-overload-induced dopamine neuron degeneration in the substantia nigra of rats

机译:硝苯地平可预防黑质中大鼠铁蓄积并逆转铁超负荷引起的多巴胺神经元变性

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Abstract The mechanisms of iron accumulation in substantia nigra (SN) of Parkinson's diseases remain unclear.The objective of this study was to investigate effects of nifedipine on iron-overload-induced iron accumulation and neurodegeneration in SN of rats. By high performance liquid chromatography- electrochemical detection, tyrosine hydroxylase (TH) immunohistochemistry, and iron content array, we first quantified iron content and the number of dopamine neurons in SN of experimental rats treated with iron dextran. We further assessed effects of treatment with nifedipine. Our results showed that nifedipine treatment prevents iron dextran- induced dopamine depletion in the striatum. Consistently, we found that nifedipine restores the number of TH-positive neurons reduced by iron dextran overload and prevents increase of iron content in the SN. These results suggested that nifedipine may suppress iron toxicity in dopamine neurons and prevent neurodegeneration.
机译:摘要帕金森氏病在黑质(SN)中铁蓄积的机制尚不清楚。本研究的目的是研究硝苯地平对铁超负荷引起的SN中铁蓄积和​​神经变性的影响。通过高效液相色谱-电化学检测,酪氨酸羟化酶(TH)免疫组织化学和铁含量阵列,我们首先量化了右旋糖酐铁治疗的实验大鼠SN中的铁含量和多巴胺神经元的数量。我们进一步评估了硝苯地平治疗的效果。我们的结果表明硝苯地平治疗可防止右旋糖酐铁引起的纹状体中多巴胺的消耗。一致地,我们发现硝苯地平可恢复右旋糖酐铁超负荷减少的TH阳性神经元的数量,并防止SN中铁含量的增加。这些结果表明硝苯地平可以抑制多巴胺神经元中的铁毒性并预防神经变性。

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