Abstract
BackgroundGlutamate, the main excitatory neurotransmitter, is involved in learning and memory processes but at higher concentration results excitotoxic causing degeneration and neuronal death. Adenosine is a nucleoside that exhibit neuroprotective effects by modulating of glutamate release. Hypoxic and related oxidative conditions, in which adenosine and metabotropic glutamate receptors are involved, have been demonstrated to contribute to neurodegenerative processes occurring in certain human pathologies.ResultsHuman neuroblastoma cells (SH-SY5Y) were used to evaluate the long time (24, 48 and 72 hours) effects of a [60]fullerene hydrosoluble derivative (t3ss) as potential inhibitor of hypoxic insult. Low oxygen concentration (5% O2) caused cell death, which was avoided by t3ss exposure in a concentration dependent manner. In addition, gene expression analysis by real time PCR of adenosine A1, A2A and A2B and metabotropic glutamate 1 and 5 receptors revealed that t3ss significantly increased A1 and mGlu1 expression in hypoxic conditions. Moreover, t3ss prevented the hypoxia-induced increase in A2A mRNA expression.ConclusionsAs t3ss causes overexpression of adenosine A1 and metabotropic glutamate receptors which have been shown to be neuroprotective, our results point to a radical scavenger protective effect of t3ss through the enhancement of these neuroprotective receptors expression. Therefore, the utility of these nanoparticles as therapeutic target to avoid degeneration and cell death of neurodegenerative diseases is suggested.
Highlights
Low oxygen availability in neuronal cells is the main cause of cognitive and physical deficiencies in patients who suffered ischemic toxicity in brain
Step was to test the possible role of t3ss on gene expression modulation of receptors involved in neurodegenerative processes and diseases, such as adenosine (AR) and metabotropic glutamate receptors [25,26,27]
Even though the treatment of SH-SY5Y cells with 75 μM t3ss derivative exhibited similar significant protective effect in both the 6 and 24 h period of hypoxia, as observed from MTT assay, in the shorter period of treatment, we did not observe any change in gene expression from qPCR
Summary
Low oxygen availability in neuronal cells is the main cause of cognitive and physical deficiencies in patients who suffered ischemic toxicity in brain. A dramatic increase in ROS has been related to cell death induced by oxidative stress and to neurodegenerative diseases as Alzheimer’s [5]. Apoptotic cell death is mainly mediated by an increase in mitochondrial permeability to calcium which promotes cytochrome c release [6]. The main excitatory neurotransmitter, is involved in learning and memory processes but at higher concentration results excitotoxic causing degeneration and neuronal death. Hypoxic and related oxidative conditions, in which adenosine and metabotropic glutamate receptors are involved, have been demonstrated to contribute to neurodegenerative processes occurring in certain human pathologies
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