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光生物调节对雄性 Sprague-Dawley 大鼠脂多糖诱导的多巴胺能神经元丢失的挽救作用。

Effect of Photobiomodulation in Rescuing Lipopolysaccharide-Induced Dopaminergic Cell Loss in the Male Sprague-Dawley Rat.

机构信息

Discipline of Anatomy & Histology, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, NSW 2006, Australia.

出版信息

Biomolecules. 2019 Aug 19;9(8):381. doi: 10.3390/biom9080381.

Abstract

Photobiomodulation (PBM) provides neuroprotection against dopaminergic cell death and associated motor deficits in rodent and primate models of Parkinson's disease (PD). However, it has not yet been tested in the lipopolysaccharide (LPS) model of PD, which leads to dopaminergic cell death through microglia-evoked neuroinflammation. We investigated whether transcranial PBM could protect against dopaminergic cell death within the substantia nigra in male Sprague-Dawley rats following supranigral LPS injection. PBM fully protected rats from 10 µg LPS which would have otherwise caused 15% cell loss, but there was no significant neuroprotection at a 20 µg dose that led to a 50% lesion. Cell loss at this dose varied according to the precise site of injection and correlated with increased local numbers of highly inflammatory amoeboid microglia. Twenty microgram LPS caused motor deficits in the cylinder, adjusted stepping and rotarod tests that correlated with dopaminergic cell loss. While PBM caused no significant improvement at the group level, motor performance on all three tests no longer correlated with the lesion size caused by 20 µg LPS in PBM-treated rats, suggesting extranigral motor improvements in some animals. These results provide support for PBM as a successful neuroprotective therapy against the inflammatory component of early PD, provided inflammation has not reached a devastating level, as well as potential benefits in other motor circuitries.

摘要

光生物调节(PBM)可提供神经保护,防止帕金森病(PD)的啮齿动物和灵长类动物模型中的多巴胺能细胞死亡和相关运动缺陷。然而,它尚未在脂多糖(LPS)诱导的 PD 模型中进行测试,该模型通过小胶质细胞引发的神经炎症导致多巴胺能细胞死亡。我们研究了经颅 PBM 是否可以防止 LPS 注射后雄性 Sprague-Dawley 大鼠黑质内的多巴胺能细胞死亡。PBM 完全保护大鼠免受 10µg LPS 的影响,否则这会导致 15%的细胞丢失,但在导致 50%损伤的 20µg 剂量下,没有明显的神经保护作用。该剂量的细胞丢失取决于注射的确切部位,并与局部高度炎症性阿米巴样小胶质细胞数量增加相关。20µg LPS 导致圆筒、调整步距和转棒测试中的运动缺陷,这与多巴胺能细胞丢失相关。虽然 PBM 在组水平上没有引起显著改善,但在 PBM 治疗的大鼠中,所有三种测试的运动性能不再与 20µg LPS 引起的损伤大小相关,这表明一些动物的黑质外运动改善。这些结果为 PBM 作为一种成功的神经保护疗法提供了支持,用于治疗早期 PD 的炎症成分,前提是炎症尚未达到破坏性水平,并且在其他运动回路中也可能有潜在益处。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ceeb/6723099/794c2be71423/biomolecules-09-00381-g001.jpg

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