相关实验视频

Updated: Feb 19, 2026

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing

Published on: June 9, 2017

氨酸通过对Nrf2和NF-κB通路的双调节来保护 gentamicin 诱导的神经毒性

Amira E Farage¹, Medhat Taha², Basma Adel Khattab³

¹Department of Anatomy and Embryology, Faculty of Medicine, Kafrelsheikh University, Kafr Elsheikh 33511, Egypt.

|February 17, 2026

概括

氨酸在老鼠中有效地保护了抗 gentamicin 诱导的神经毒性. 它改善了行为,减少了大脑损伤,氧化应激,炎症和亡,突出了其神经保护潜力.

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.
毒理学毒理学毒理学

背景情况:

抗生素 جنت米辛 (GM) 可以引起神经毒性,导致认知和行为缺陷.
氨酸Taurine具有已知的神经保护性质.
了解 taurine 在缓解 gentamicin 诱导的神经毒性的作用对于开发治疗策略至关重要.

研究的目的:

在斯普雷格·道利大鼠中研究 taurine 对 gentamicin 诱导的神经毒性的神经保护作用.
评估 taurine 在 gentamicin 暴露后对行为,海马体结构,氧化应激,神经炎症和亡的影响.

主要方法:

三十二只老鼠被分为对照组,牛素, gentamicin (GM) 和牛素+GM组.
行为测试 (开放场,Y迷宫) 评估了运动运动活动,焦虑和记忆.
河马组织通过组织病理学,免疫组织化学,ELISA和RT-qPCR进行分析.

主要成果:

转基因的使用引起了焦虑,海马体退化,氧化应激 (增加MDA,减少SOD/CAT),神经炎症 (增加NF-B,TNF-α,IL-1β,IL-6) 和亡 (增加caspase-3,Bax;减少Bcl-2).
氨酸联合治疗逆转了这些转基因诱导的效应,改善了行为并保持了神经元的完整性.
氨酸恢复了抗氧化防御 (Nrf2/HO-1通路),抑制了炎症,并调节了亡标志物.

结论:

氨酸在老鼠中表现出显著的神经保护作用,防止 gentamicin 的毒性.
它的机制包括增强抗氧化能力,减少神经炎症和抑制神经元亡.
氨酸作为治疗 gentamicin 诱导的神经毒性的治疗剂具有前景.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.药物诱导的神经毒性药物诱导的神经毒性这是一种 gentamicin.炎症炎症是一种炎症.氧化压力是一种氧化压力.氨酸 (Taurine) 是一种氨酸.

更多相关视频

Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis

Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis

Published on: February 13, 2014

Strategies for Study of Neuroprotection from Cold-preconditioning

Strategies for Study of Neuroprotection from Cold-preconditioning

Published on: September 2, 2010

相关概念视频

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...

NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...

Drugs Affecting Neurotransmitter Synthesis

Drugs Affecting Neurotransmitter Synthesis

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,...

Enzyme-linked Receptors

Enzyme-linked Receptors

Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

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...