科伊克索尔通过抑制神经炎症和保护线粒体功能来改善多巴氨基性神经退行症
Shuo Yang1,2, Jiaxi Han1, Miao Xue1
1State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.
Frontiers in pharmacology
|October 20, 2025
概括
来自Coix lacryma-jobi L.的Coixol通过减少神经炎症和保护线粒体来缓解帕金森病 (PD) 的症状. 这种天然化合物抑制了关键的炎症途径,为PD提供了潜在的治疗途径.
科学领域:
- 神经科学是一个神经科学.
- 药理学 药理学是指药理学的学科.
- 免疫学 免疫学 免疫学
背景情况:
- 神经炎症是帕金森病 (PD) 发病的一个重要因素.
- 科伊克索尔是一种来自Coix lacryma-jobi L.的化合物,具有已知的抗炎和抗氧化特性.
- 在PD中,coixol的治疗潜力以前没有被研究过.
研究的目的:
- 在帕金森病的动物模型中评估coixol的疗效.
- 阐明coixol在PD中发挥作用的潜在机制.
主要方法:
- 使用了一种由1-甲基-4--1,2,3,6-四胺 (MPTP) 诱导的帕金森病小鼠模型.
- 评估运动功能,神经元损伤和神经炎症标志物.
- 研究了醇对核转录因子 κB (NF-κB),基因激活蛋白激酶 (MAPK) 和NLRP3炎症酶信号通路的影响.
- 测量了活性氧物种 (ROS) 水平和线粒体功能.
主要成果:
- 在接受MPTP治疗的小鼠中,Coixol治疗显著改善了运动功能障碍,并减少了神经元损伤.
- 科伊索尔抑制NF-κB和MAPK信号通路的激活,从而抑制神经炎症.
- 科伊索尔调节了NLRP3/Caspase1/IL-1β通路,并减轻了ROS诱导的线粒体损伤,抑制了NLRP3炎症酶过度激活.
结论:
- 科伊索尔在帕金森病的小鼠模型中显示出神经保护作用.
- 醇的治疗效益通过抑制神经炎症信号通路 (NF-κB,MAPK,NLRP3炎症体) 来实现.
- 科伊索尔可以保护线粒体功能免受ROS损伤,这表明它有可能成为帕金森病的新型治疗剂.
相关概念视频
Drugs Affecting Neurotransmitter Synthesis
2.1K
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
2.1K
Alzheimer's Disease: Treatment
811
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
811
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists
552
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
552
Electron Transport Chain: Complex I and II
18.4K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
ROS generation is regulated and maintained at moderate levels necessary...
18.4K
Drugs Affecting Neurotransmitter Release or Uptake
1.5K
Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
1.5K
Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein
814
Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
814


