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Neurotoxicity of quinolinic acid to Spiral Ganglion Cells in Rats

Journal of Huazhong University of Science and Technology(Medical Sciences) 2010年第3期30卷 397-402页

作者：肖红俊杨琛何圆圆郑娜 Department of Otorhinolaryngology Union HospitalTongji Medical CollegeHuazhong University of Science and Technology

Our study investigated the neurotoxicity of quinolinic acid(QA) to spiral ganglion cells(SGCs),observed the protective effects of N-methyl-D-aspartate(NMDA) receptor antagonist MK-801 and magnesium ions on the QA-induced injury to SGCs,and analyzed the role of QA in otitis media with effusion(OME)-induced sensorineural hearing loss(SNHL).After culture in vitro for 72 h,SGCs were exposed to different media and divided into 4 groups:the blank control group,the QA injury group,the MK-801 treatment group,and the MgCl2 protection *** apoptosis rate of SGCs was analyzed by Annexin V and PI double staining under the fluorescence microscopy 24 h *** were cultured in vitro for 72 h and divided into four groups:the low concentration QA group,the high concentration QA group,the MK-801 group,the MgCl2 *** transient changes of intracellular calcium concentration were observed by the laser scanning confocal *** rate in QA injury group was higher than that in blank control group and MgCl2 protection group(both P0.05).In high concentration QA group,there was an obvious increase of the intracellular calcium concentration in SGCs,which didn’t present in low concentration QA *** MgCl2 group,the peak values of the intracellular calcium concentration in SGCs were reduced and the duration was shortened,but the intracellular calcium concentration in SGCs had no significant change in MK-801 *** was concluded that QA could injure SGCs by excessively activating NMDA receptors on the cell membrane,which might be the mechanism by which OME induced SNHL,while Mg2+ could protect the SCGs from the neurotoxicity of QA.

关键词： quinolinic acid neurotoxicity otitis media with effusion sensorineural hearing loss

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Research progress of quinolinic acid in neuropsychiatric diseases

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Journal of Hainan Medical University 2020年第16期26卷 74-78页

作者： Xiao-Yu Guo Yan-Qing Han Wei Lv Department of Neurology Second Hospital of Shanxi Medical UniversityTaiyuan 030000ShanxiChina Shanxi Cardiovascular Hospital Shanxi Medical UniversityTaiyuan 030000ShanxiChina

quinolinic acid is a neurotoxic substance produced by tryptophan through the kynurenine metabolism *** acid is involved in the pathological processes of Alzheimer's disease,Parkinson's disease,Huntington's disease,amyotrophic lateral sclerosis,encephalitis,depression,and *** above process is realized through pathophysiological processes such as excitatory neurotoxicity,metabolic damage,free radical generation and oxidative stress,participation in inflammatory response,induction of neuron and astrocytic *** article will explain the metabolic regulation,biological characteristics,and neurotoxicity of quinolinic *** research progress of quinolinic acid in Alzheimer's disease,Parkinson's disease,Huntington's disease,depression and subacute sclerosing panencephalitis is also described.

关键词： quinolinic acid Ynurenine metabolic pathway Eurodegenerative disease

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Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2

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Neural Regeneration Research 2025年第6期20卷 1776-1788页

作者： Zige Jiang Dexiang Liu Tingting Li Chengcheng Gai Danqing Xin Yijing Zhao Yan Song Yahong Cheng Tong Li Zhen Wang Department of Physiology School of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Medical Psychology and Ethics School of Basic Medicine SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Neurosurgery Surgery Qingdao Municipal HospitalQingdaoShandong ProvinceChina

The pathophysiology of Huntington's disease involves high levels of the neurotoxin quinolinic acid. quinolinic acid accumulation results in oxidative stress, which leads to neurotoxicity. However, the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington's disease pathology remain unknown. In this study, we established in vitro and in vivo models of Huntington's disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice, respectively. We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum, which was accompanied by down-regulation of cystathionine β-synthase, an enzyme responsible for hydrogen sulfide production. However, treatment with NaHS(a hydrogen sulfide donor) increased hydrogen sulfide levels in the neurons and in mouse serum, as well as cystathionine β-synthase expression in the neurons and the mouse striatum, while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum. These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression. Finally, treatment with the nuclear factor erythroid 2-related factor 2inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress. Taken together, our findings show that hydrogen sulfide reduces oxidative stress in Huntington's disease by activating nuclear factor erythroid 2-related factor 2,suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington's disease.

关键词： apoptosis cystathionine-β-synthase nuclear factor erythroid 2-related factor 2 Huntington's disease hydrogen sulfide mitochondrion neuroplasticity oxidative stress quinolinic acid reactive oxygen species

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Eleutheroside B or E enhances learning and memory in experimentally aged rats

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Neural Regeneration Research 2013年第12期8卷 1103-1112页

作者： Debin Huang Zehua Hu Zhaofen Yu Department of Pharmacology Hubei Institute for Nationalities

Eleutheroside B or E, the main component of Acanthopanax, can relieve fatigue, enhance memory, and improve human cognition. Numerous studies have confirmed that high doses of acetylcholine significantly attenuate clinical symptoms and delay the progression of Alzheimer＇s disease. The present study replicated a rat model of aging induced by injecting quinolinic acid into the hippocampal CA1 region. These rats were intraperitoneally injected with low, medium and high doses of eleutheroside B or E （50, 100, 200 mg/kg）, and rats injected with Huperzine A or PBS were used as controls. At 4 weeks after administration, behavioral tests showed that the escape latencies and errors in searching for the platform in a Morris water maze were dose-dependently reduced in rats treated with medium and high-dose eleutheroside B or E. Hematoxylin-eosin staining showed that the number of surviving hippocampal neurons was greater and pathological injury was milder in three eleutheroside B or E groups compared with model group. Hippocampal homogenates showed enhanced cholinesterase activity, and dose-dependent increases in acetylcholine content and decreases in choline content following eleutheroside B or E treatment, similar to those seen in the Huperzine A group. These findings indicate that eleutheroside B or E improves learning and memory in aged rats. These effects of eleutheroside B or E may be mediated by activation of cholinesterase or enhanced reuse of choline to accelerate the synthesis of acetylcholine in hippocampal neurons.

关键词： neural regeneration traditional Chinese medicine eleutheroside B or E quinolinic acid aged rats Huperzine A learning and memory hippocampus acetylcholine cholinesterase choline mechanism grants-supported paper neuroregeneration

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Inhibiting the kynurenine pathway in spinal cord injury: multiple therapeutic potentials?

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Neural Regeneration Research 2018年第12期13卷 2073-2076页

作者： Kelly R.Jacobs David B.Lovejoy Neuroinflammation Group Centre for Motor Neuron Disease Research Department of Biomedical Sciences Faculty of Medicine and Health Sciences Macquarie University

Chronic induction of the kynurenine pathway（KP） contributes to neuroinflammation by producing the excitotoxin quinolinic acid（QUIN）. This has led to significant interest in the development of inhibitors of this pathway, particularly in the context of neurodegenerative disease. However, acute spinal cord injury（SCI） also results in deleterious increases in QUIN, as secondary inflammatory processes mediated largely by infiltrating macrophages, become predominant. QUIN mediates significant neurotoxicity primarily by excitotoxic stimulation of the N-methyl-D-aspartate receptor, but other mechanisms of QUIN toxicity are known. More recent focus has assessed the contribution that neuroinflammation and modulations in the KP make in mood and psychiatric disorders with recent studies linking inflammation and modulations in the KP, to impaired cognitive performance and depressed mood in SCI patients. We hypothesize that these findings suggest that in SCI, inhibition of QUIN production and other metabolites, may have multiple therapeutic modalities and further studies investigating this are warranted. However, for central nervous system-based conditions, achieving good blood-brain-barrier permeability continues to be a limitation of current KP inhibitors.

关键词： spinal cord injury neuroinflammation kynurenine pathway activated microglia infiltrating macrophages quinolinic acid neuropsychiatry depression

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Alpha-7 nicotinic acetylcholine receptor agonist treatment in a rat model of Huntington's disease and involvement of heme oxygenase-1

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Neural Regeneration Research 2018年第4期13卷 737-741页

作者： Laura Foucault-Fruchard Claire Tronel Sylvie Bodard Zuhal Gulhan Julie Busson Sylvie Chalon Daniel Antier UMR 1253 iBrainUniversité de Tours CHRU de Tours H?pital Bretonneau

Neuroinflammation is a common element involved in the pathophysiology of neurodegenerative *** recently reported that repeated alpha-7 nicotinic acetylcholine receptor（α7 n ACh R） activations by a potent agonist such as PHA 543613 in quinolinic acid-injured rats exhibited protective effects on *** further investigate the underlying mechanism,we established rat models of early-stage Huntington＇s disease by injection of quinolinic acid into the right striatum and then intraperitoneally injected 12 mg/kg PHA 543613 or sterile water,twice a day during 4 *** blot assay results showed that the expression of heme oxygenase-1（HO-1）,the key component of the cholinergic anti-inflammatory pathway,in the right striatum of rat models of Huntington＇s disease subjected to intraperitoneal injection of PHA 543613 for 4 days was significantly increased compared to the control rats receiving intraperitoneal injection of sterile water,and that the increase in HO-1 expression was independent of change in α7 n ACh R *** findings suggest that HO-1 expression is unrelated to α7 n ACh R density and the increase in HO-1 expression likely contributes to α7 n ACh R activation-related neuroprotective effect in early-stage Huntington＇s disease.

关键词： alpha 7 nicotinic receptor PHA 543613 quinolinic acid cholinergic anti-inflammatory pathway neuroinflammation neurodegenerative disease

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