Treadmill intervention attenuates motor deficit with 6-OHDA-induced Parkinson's disease rat via changes in lipid profiles in brain and muscle.

IF 3.9 3区 医学 Q2 CELL BIOLOGY
Aging-Us Pub Date : 2025-01-03 DOI:10.18632/aging.206181
Binar Panunggal, Tu-Hsueh Yeh, Shu-Ping Tsao, Chun-Hsu Pan, Wei-Ting Shih, Ya-Tin Lin, Amelia Faradina, Chia-Lang Fang, Hui-Yu Huang, Shih-Yi Huang
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Abstract

One of the key hallmarks of Parkinson's disease is the disruption of lipid homeostasis in the brain, which plays a critical role in neuronal membrane integrity and function. Understanding how treadmill training impacts lipid restructuring and its subsequent influence on motor function could provide a basis for developing targeted non-pharmacological interventions for individuals living with early stage of PD. This study aims to investigate the effects of a treadmill training intervention on motor deficits induced by 6-OHDA in rats model of PD. PD was induced by injecting 6-hydroxy dopamine (6-OHDA) into the medial forebrain bundle (MFB). For 10 weeks, rats underwent treadmill training on a four-lane motorized treadmill. Motor function deficits were evaluated through behavioral tests. Lipidomic analysis was performed through ultrahigh-performance liquid chromatography-tandem mass spectrometry (UPLC MS/MS). Treadmill intervention significantly improved motor function and restored altered brain and muscle lipid profiles in PD rats. Among the lipid species identified in PD rats, brain abundance was highest for phosphatidylethanolamine (PE), correlating positively with the beam-walking scores; muscle abundance peaked with lysophosphatidylethanolamine (LysoPE), correlating positively with grip strength scores. In the brain, the levels of diacylglycerol (DG), triacylglycerol (TG), and lysophosphatidylcholine (PC) correlated positively with grip strength and rotarod scores, while only phosphatidylethanolamine (PE) linked to beam-walking scores. In the muscle, the levels of phosphatidylinositol (PI), lysophosphatidylethanolamine (PE), lysophosphatidic acid (PA), ceramide (Cer), and ganglioside were positively correlated with grip strength and rotarod scores. In conclusion, treadmill may protect the cortex, mitigating motor deficits via change lipid profiles in the brain and muscle.

跑步机干预通过改变脑和肌肉脂质谱减轻6-羟多巴胺诱导的帕金森病大鼠的运动缺陷。
帕金森病的一个关键特征是大脑脂质稳态的破坏,这在神经元膜的完整性和功能中起着关键作用。了解跑步机训练如何影响脂质重组及其随后对运动功能的影响,可以为开发针对早期PD患者的有针对性的非药物干预提供基础。本研究旨在探讨跑步机训练干预对6-羟多巴胺诱导的PD大鼠运动功能障碍的影响。将6-羟基多巴胺(6-OHDA)注入内侧前脑束(MFB)诱导PD。大鼠在四车道的电动跑步机上进行了10周的跑步训练。通过行为测试评估运动功能缺陷。脂质组学分析采用超高效液相色谱-串联质谱(UPLC MS/MS)。跑步机干预显著改善了PD大鼠的运动功能,并恢复了改变的脑和肌肉脂质谱。在PD大鼠所鉴定的脂质种类中,磷脂酰乙醇胺(PE)的脑丰度最高,与beam-walking评分呈正相关;肌肉丰度在溶血磷脂酰乙醇胺(LysoPE)中达到峰值,与握力评分呈正相关。在大脑中,二酰基甘油(DG)、三酰基甘油(TG)和溶磷脂酰胆碱(PC)的水平与握力和旋转杆得分呈正相关,而只有磷脂酰乙醇胺(PE)与束走得分相关。在肌肉中,磷脂酰肌醇(PI)、溶血磷脂酰乙醇胺(PE)、溶血磷脂酸(PA)、神经酰胺(Cer)和神经节苷脂的水平与握力和旋转杆评分呈正相关。总之,跑步机可以保护大脑皮层,通过改变大脑和肌肉的脂质谱来减轻运动缺陷。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Aging-Us
Aging-Us CELL BIOLOGY-
CiteScore
10.00
自引率
0.00%
发文量
595
审稿时长
6-12 weeks
期刊介绍: Information not localized
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