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Caffeic acid phenethyl ester blocks free radical generation and 6-hydroxydopamine-induced neurotoxicity.

机译:咖啡酸苯乙酯可阻止自由基的产生和6-羟基多巴胺诱导的神经毒性。

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Neurotoxicity induced by 6-hydroxydopamine (6-OHDA) is believed to be due, in part, to the production of reactive oxygen species (ROS). Antioxidants protect neurons against 6-OHDA-induced neurotoxicity by inhibiting free radical generation. In this study, we investigated whether or not caffeic acid phenethyl ester (CAPE) could protect neurons against 6-OHDA-induced neurotoxicity in cultured rat rostral mesencephalic neurons (RMN) and cerebellar granule neurons (CGN). We now report that exposure of RMN and CGN to 6-OHDA (40 microM for RMN and 70 microM for CGN) resulted in significant increases in free radical production and death of both neuron types. Pretreatment with CAPE (10 microM) for 2 h prevented both 6-OHDA-induced free radical generation and neurotoxicity. Furthermore, CAPE also attenuated H(2)O(2)-induced neurotoxicity. Our results strongly suggest that CAPE blocks 6-OHDA-induced neuronal death possibly by inhibiting 6-OHDA-induced free radical generation and blocking free radical-induced neurotoxicity in neurons. Both the antioxidative and neuroprotective effects of CAPE may be beneficial in the therapy for Parkinson's disease and other neurodegenerative diseases.
机译:据信由6-羟基多巴胺(6-OHDA)引起的神经毒性部分归因于活性氧(ROS)的产生。抗氧化剂通过抑制自由基的产生,保护神经元免受6-OHDA诱导的神经毒性。在这项研究中,我们调查了咖啡酸苯乙酯(CAPE)是否能保护神经元免受6-OHDA诱导的培养的大鼠鼻中脑神经元(RMN)和小脑颗粒神经元(CGN)的神经毒性。我们现在报告,RMN和CGN暴露于6-OHDA(RMN为40 microM,CGN为70 microM)导致两种神经元类型的自由基产生和死亡显着增加。用CAPE(10 microM)预处理2 h可以防止6-OHDA诱导的自由基生成和神经毒性。此外,CAPE还减弱了H(2)O(2)诱导的神经毒性。我们的结果强烈表明,CAPE可能通过抑制6-OHDA诱导的自由基生成并阻断神经元中的自由基诱导的神经毒性来阻断6-OHDA诱导的神经元死亡。 CAPE的抗氧化和神经保护作用在帕金森氏病和其他神经退行性疾病的治疗中可能都是有益的。

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