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Int J Biol Macromol ; 164: 1099-1111, 2020 Dec 01.
Article in English | MEDLINE | ID: mdl-32629049

ABSTRACT

Neurodegenerative diseases are characterized by progressive loss of neurons in the central nervous system (CNS). Several molecules play a role in mammalian CNS regeneration, including glycosaminoglycans (GAGs). GAGs are found in abundance in many marine invertebrates, such as ascidians that belong to the phylum Chordata, which show a high CNS regeneration capacity even in adulthood. Here, we investigated the roles of dermatan sulfate, a type of GAG that was obtained from the ascidian Phallusia nigra. We investigated the neuroprotective and antioxidant properties of Phallusia nigra dermatan sulfate (PnDS) after neurotoxic damage induced by the pesticide rotenone using the Neuro-2A cell lineage. Neuroprotection was observed through a mitochondrial activity analysis. A morphometric analysis revealed long unbranched neurites after incubation with PnDS and co-incubation with PnDS and rotenone. Furthermore, PnDS showed antioxidant activity that reduced reactive oxygen species (ROS) even in co-incubation with rotenone. The reduced ROS probably occurred because PnDS increased the activity of the antioxidant enzymes superoxide dismutase and catalase and improved total antioxidant capacity, which protected cells from damage, as observed through decreased levels of lipid peroxidation. These data suggest a neuroprotective and antioxidant role of PnDS even under neurodegenerative conditions caused by rotenone.


Subject(s)
Antioxidants/pharmacology , Brain Neoplasms/drug therapy , Dermatan Sulfate/pharmacology , Neuroblastoma/pathology , Neuroprotective Agents/pharmacology , Urochordata/chemistry , Animals , Antioxidants/isolation & purification , Cell Line, Tumor , Cell Lineage , Cell Survival/drug effects , Dermatan Sulfate/isolation & purification , Glycosaminoglycans/chemistry , Lipid Peroxidation , Mice , Microscopy, Electron, Scanning , Neuroprotective Agents/isolation & purification , Reactive Oxygen Species/metabolism , Regeneration , Rotenone , Signal Transduction
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