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Astrocytes and retrograde degeneration of nigrostriatal dopaminergic neurons in Parkinson’s disease:removing axonal debris

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Translational Neurodegeneration 2021年第4期10卷 554-572页

作者： ingrid morales Ricardo Puertas-Avendaño Alberto Sanchez Adrian Perez-Barreto Clara Rodriguez-Sabate Manuel Rodriguez Laboratory of Neurobiology and Experimental Neurology Department of Basic Medical SciencesFaculty of MedicineLa Laguna UniversityLa LagunaTenerifeCanary IslandsSpain Center for Networked Biomedical Research on Neurodegenerative Diseases(CIBERNED) MadridSpain

Objective:The dopaminergic nigrostriatal neurons(DA cells)in healthy people present a slow degeneration with aging,which produces cellular debris throughout *** 2%-5%of people present rapid cell degeneration of more than 50%of DA cells,which produces Parkinson's disease(PD).Neuroinflammation accelerates the cell degeneration and may be critical for the transition between the slow physiological and the rapid pathological degeneration of DA cells,particularly when it activates microglial cells of the medial forebrain bundle near dopaminergic *** synaptic debris produced by DA cell degeneration may trigger the parkinsonian neuroinflammation,this study investigated the removal of axonal debris produced by retrograde degeneration of DA cells,paying particular attention to the relative roles of astrocytes and ***:Rats and mice were injected in the lateral ventricles with 6-hydroxydopamine,inducing a degeneration of dopaminergic synapses in the striatum which was not accompanied by non-selective tissue damage,microgliosis or *** possible retrograde degeneration of dopaminergic axons,and the production and metabolization of DA-cell debris were studied with immunohistochemical methods and analyzed in confocal and electron microscopy ***:The selective degeneration of dopaminergic synapses in the striatum was followed by a retrograde degeneration of dopaminergic axons whose debris was found within spheroids of the medial forebrain *** spheroids retained mitochondria and most(e.g.,tyrosine hydroxylase,the dopamine transporter protein,and amyloid precursor protein)but not all(e.g.,α-synuclein)proteins of the degenerating dopaminergic *** showed initial(autophagosomes)but not late(lysosomes)components of autophagy(incomplete autophagy).These spheroids were penetrated by astrocytic processes of the medial forebrain bundle,which provided the lysosomes needed to continue the degradation of dopaminergic debri

关键词： Astrocyte Phagocytosis Parkinson's disease Dying-back degeneration Medial forebrain bundle Spheroid

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Protective effect of some vitamins against the toxic action of ethanol on liver regeneration induced by partial hepatectomy in rats

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World Journal of Gastroenterology 2008年第6期14卷 899-907页

作者： Carlett Ramírez-Farías Eduardo Madrigal-Santillán José Gutiérrez-Salinas Nidia Rodríguez-Sánchez Maricela Martínez-Cruz Ilse Valle-Jones ingrid Gramlich-Martínez Alejandra Hernández-Ceruelos José A morales-González Unidad de Genética de la Nutrición Instituto Nacional de Pediatría México Instituto de Ciencias de la Salud Universidad Autónoma del Estado de Hidalgo México Laboratorio de Bioquímica y Medicina Experimental Unidad de Investigación Biomédica División de Investigación Centro Médico Nacional "20 de Noviembre" ISSSTE México Gatorade Sports Science Institute Mexico City México Escuela de Dietética y Nutrición ISSSTE México University of Ryerson Toronto

AIM: To investigate the effects of vitamins (A, C and E) on liver injury induced by ethanol administration during liver regeneration in rats. METHODS: Male Wistar rats subjected to 70% partial hepatectomy were divided into five groups (groups 1-5). During the experiment, animals of Group 1 drank only water. The other four groups (2-5) drank 30 mL of ethanol/L of water. Group 3 additionally received vitamin A, those of group 4 vitamin C and those of group 5 received vitamin E. Subsequently serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin and bilirubin were measured colorimetrically. Lipid peroxidation (thiobarbituric-acid reactive substances, TBARS) both in plasma and liver was measured, as well as liver mass gain assessment and total DNA. RESULTS: Compared with sham group, serum AST and ALT increased significantly under ethanol treatment (43% and 93%, respectively, with P < 0.05). Vitamin C and vitamin E treatment attenuated the ethanol-induced increases in ALT and AST activity. Ethanol treatment also decreased serum albumin concentration compared to sham group (3.1 ± 0.4 g/dL vs 4.5 ± 0.2 g/dL; P < 0.05). During liver regeneration vitamins C and E significantly ameliorated liver injury for ethanol administration in hepatic lipid peroxidation (4.92 nmol/mg and 4.25 nmol/mg vs 14.78 nmol/mg, respectively, with P < 0.05). In association with hepatic injury, ethanol administration caused a significant increase in both hepatic and plasma lipid peroxidation. Vitamins (C and E) treatment attenuated hepatic and plasma lipid peroxidation. CONCLUSION: Vitamins C and E protect against liver injury and dysfunction, attenuate lipid peroxidation, and thus appear to be significantly more effective than vitamin A against ethanol-mediated toxic effects during liver regeneration.

关键词： Lipid peroxidation Antioxidant vitamins Alcohol-induced liver injury Liver regeneration

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