关键词: Cobalt Ferrite Nanoparticles NPs Neurotransmitters Parkinson Disease ZnO Nanoparticles

Mesh : Animals Zinc Oxide / pharmacology chemistry Mice Rotenone Neuroprotective Agents / pharmacology Disease Models, Animal Male Nanoparticles / chemistry Ferric Compounds / pharmacology Parkinson Disease / drug therapy metabolism Dopamine / metabolism Cobalt / pharmacology

来  源:   DOI:10.7150/ntno.95863   PDF(Pubmed)

Abstract:
Goals of the investigation: This work aimed to evaluate the neuroprotective effects of zinc oxide (ZnO) nanoparticles in an experimental mouse model of rotenone-induced PD and investigate the therapeutic effects of ZnO, cobalt ferrite nanoparticles, and their combination. Methods: The levels of dopamine, norepinephrine, epinephrine, and serotonin were assessed using ELISA in the control and experimental model of PD mice. The dopa-decarboxylase expression level was assayed by real-time PCR. The expression level of tyrosine hydroxylase (TH) was assessed by western blot analysis. Results: Our data showed that levels of dopamine decreased in PD mice compared to normal. ZnO NP increased dopamine levels in normal and PD mice (37.5% and 29.5%; respectively, compared to untreated mice). However, ZnO NP did not cause any change in norepinephrine and epinephrine levels either in normal or in PD mice. Levels of serotonin decreased by 64.0%, and 51.1% in PD mice treated with cobalt ferrite and dual ZnO- cobalt ferrite NPs; respectively, when compared to PD untreated mice. The mRNA levels of dopa-decarboxylase increased in both normal and PD mice treated with ZnO NP. Its level decreased when using cobalt ferrite NP and the dual ZnO-cobalt ferrite NP when compared to untreated PD mice. A significant decrease in TH expression by 0.25, 0.68, and 0.62 folds was observed in normal mice treated with ZnO, cobalt ferrite, and the dual ZnO-cobalt ferrite NP as compared to normal untreated mice. In PD mice, ZnO administration caused a non-significant 0.15-fold decrease in TH levels while both cobalt ferrite and the dual ZnO-cobalt ferrite NP administration caused a significant 0.3 and 0.4-fold decrease respectively when compared to untreated PD mice. Principal conclusion: This study reveals that ZnO NPs may be utilized as a potential intervention to elevate dopamine levels to aid in PD treatment.
摘要:
研究目标:这项工作旨在评估氧化锌(ZnO)纳米颗粒在鱼藤酮诱导的PD实验小鼠模型中的神经保护作用,并研究ZnO的治疗作用。钴铁氧体纳米颗粒,和他们的组合。方法:多巴胺的水平,去甲肾上腺素,肾上腺素,在PD小鼠的对照和实验模型中使用ELISA评估5-羟色胺。通过实时PCR测定多巴脱羧酶表达水平。通过蛋白质印迹分析评估酪氨酸羟化酶(TH)的表达水平。结果:我们的数据显示,与正常相比,PD小鼠的多巴胺水平降低。ZnONP增加正常和PD小鼠的多巴胺水平(分别为37.5%和29.5%;与未经处理的小鼠相比)。然而,ZnONP在正常或PD小鼠中均未引起去甲肾上腺素和肾上腺素水平的任何变化。5-羟色胺水平下降64.0%,在用钴铁氧体和双ZnO-钴铁氧体NP处理的PD小鼠中,分别为51.1%;与未处理的PD小鼠相比。在用ZnONP处理的正常和PD小鼠中,多巴脱羧酶的mRNA水平均增加。与未处理的PD小鼠相比,当使用钴铁氧体NP和双ZnO-钴铁氧体NP时,其水平降低。在用ZnO处理的正常小鼠中观察到TH表达显著降低0.25、0.68和0.62倍,钴铁氧体,和与正常未处理的小鼠相比的双ZnO-钴铁氧体NP。在PD小鼠中,与未处理的PD小鼠相比,ZnO给药导致TH水平无明显的0.15倍下降,而钴铁氧体和双ZnO-钴铁氧体NP给药分别导致0.3和0.4倍下降。主要结论:这项研究表明,ZnONP可以用作潜在的干预措施,以提高多巴胺水平,以帮助PD治疗。
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