【摘 要】
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Objective To investigate whether nifedipine, a blocker of L-type calcium channels can prevent iron accumulation and dopamine neuron degeneration in the substantia nigra (SN) of acute and chronic iron-
【机 构】
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Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neuro
【出 处】
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中国神经科学学会第九届全国学术会议暨第五届会员代表大会
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Objective To investigate whether nifedipine, a blocker of L-type calcium channels can prevent iron accumulation and dopamine neuron degeneration in the substantia nigra (SN) of acute and chronic iron-overloaded rats.Methods The changes of tyrosine hydroxylase (TH) gene expression in the substantia nigra (SN) were detected by reverse transcription-polymerase chain reaction (RT-PCR), the TH-positive neurons were tested by TH immunohistochemistry, the dopamine content was measured by liquid chromatography-electrochemical detection and the iron contents of SN were determined by iron concentration assay.Results Compared with the control group, the expressions of TH mRNA decreased, and the iron contents increased in the acute iron-overloaded SN of rats.Cotreatment with nifedipine may partly restore these changes.While in the chronic iron-overloaded rats, the dopamine content in the striatum decreased after iron dextran treatment, which could be restored by nifedipine.Iron dextran overload increased iron content in the SN and reduced the number of TH-positive neurons.Treatment with nifedipine prevented the increased iron content and restored the numbers of TH-positive neurons to control values.Conclusion Nifedipine may inhibit iron-overload induced dopamine neuron damage in the iron-overloaded rats by suppressing iron toxicity.
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