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纳米载体递送 dl-3-正丁基苯酞联合针对α-突触核蛋白的抗体增强了应激诱导的帕金森病神经保护作用。

Nanowired delivery of dl-3-n-butylphthalide with antibodies to alpha synuclein potentiated neuroprotection in Parkinson's disease with emotional stress.

机构信息

Department of Neurology, Bethune International Peace Hospital, Zhongshan Road (West), Shijiazhuang, Hebei Province, P.R. China.

International Experimental Central Nervous System Injury & Repair (IECNSIR), Dept. of Surgical Sciences, Anesthesiology & Intensive Care Medicine, Uppsala University Hospital, Uppsala University, Uppsala, Sweden.

出版信息

Int Rev Neurobiol. 2023;171:47-82. doi: 10.1016/bs.irn.2023.06.005. Epub 2023 Jul 20.

DOI:10.1016/bs.irn.2023.06.005
PMID:37783563
Abstract

Stress is one of the most serious consequences of life leading to several chronic diseases and neurodegeneration. Recent studies show that emotional stress and other kinds of anxiety and depression adversely affects Parkinson's disease symptoms. However, the details of how stress affects Parkinson's disease is still not well known. Traumatic brain injury, stroke, diabetes, post-traumatic stress disorders are well known to modify the disease precipitation, progression and persistence. However, show stress could influence Parkinson's disease is still not well known. The present investigation we examine the role of immobilization stress influencing Parkinson's disease brain pathology in model experiments. In ore previous report we found that mild traumatic brain injury exacerbate Parkinson's disease brain pathology and nanodelivery of dl-3-n-butylphthalide either alone or together with mesenchymal stem cells significantly attenuated Parkinson's disease brain pathology. In this chapter we discuss the role of stress in exacerbating Parkinson's disease pathology and nanowired delivery of dl-3-n-butylphthalide together with monoclonal antibodies to alpha synuclein (ASNC) is able to induce significant neuroprotection. The possible mechanisms of dl-3-n-butylphthalide and ASNC induced neuroprotection and suitable clinical therapeutic strategy is discussed.

摘要

压力是导致多种慢性疾病和神经退行性变的最严重的生活后果之一。最近的研究表明,情绪压力和其他类型的焦虑和抑郁会对帕金森病症状产生不利影响。然而,压力如何影响帕金森病的细节尚不清楚。创伤性脑损伤、中风、糖尿病、创伤后应激障碍是众所周知的可以改变疾病的发生、进展和持续。然而,表明压力会影响帕金森病的机制仍不清楚。本研究通过模型实验,研究了固定应激对帕金森病脑病理学的影响。在之前的一份报告中,我们发现轻度创伤性脑损伤会加重帕金森病的脑病理学,而 dl-3-正丁基苯酞单独或与间充质干细胞联合的纳米传递则显著减轻帕金森病的脑病理学。在这一章中,我们讨论了应激在加重帕金森病病理学中的作用,以及 dl-3-正丁基苯酞和抗α-突触核蛋白(ASNC)单克隆抗体的纳米传递能够诱导显著的神经保护作用。讨论了 dl-3-正丁基苯酞和 ASNC 诱导神经保护的可能机制以及合适的临床治疗策略。

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1
Nanowired delivery of dl-3-n-butylphthalide with antibodies to alpha synuclein potentiated neuroprotection in Parkinson's disease with emotional stress.纳米载体递送 dl-3-正丁基苯酞联合针对α-突触核蛋白的抗体增强了应激诱导的帕金森病神经保护作用。
Int Rev Neurobiol. 2023;171:47-82. doi: 10.1016/bs.irn.2023.06.005. Epub 2023 Jul 20.
2
Co-administration of Nanowired DL-3-n-Butylphthalide (DL-NBP) Together with Mesenchymal Stem Cells, Monoclonal Antibodies to Alpha Synuclein and TDP-43 (TAR DNA-Binding Protein 43) Enhance Superior Neuroprotection in Parkinson's Disease Following Concussive Head Injury.纳米载体 DL-3-正丁基苯酞(DL-NBP)与间充质干细胞、抗α-突触核蛋白和 TDP-43(TAR DNA 结合蛋白 43)单克隆抗体联合应用可增强创伤性脑损伤后帕金森病的卓越神经保护作用。
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