Abstract
Neuroprotection from oxidative stress is critical during neuronal development and maintenance but also plays a major role in the pathogenesis and potential treatment of various neurological disorders and neurodegenerative diseases. Emerging evidence in the murine system suggests neuroprotective effects of blood plasma on the aged or diseased brain. However, little is known about plasma-mediated effects on human neurons. In the present study, we demonstrate the neuroprotective effect mediated by human plasma and the most abundant plasma–protein human serum albumin against oxidative stress in glutamatergic neurons differentiated from human neural crest-derived inferior turbinate stem cells. We observed a strong neuroprotective effect of human plasma and human serum albumin against oxidative stress-induced neuronal death on the single cell level, similar to the one mediated by tumor necrosis factor alpha. Moreover, we detected neuroprotection of plasma and human serum albumin against kainic acid-induced excitatory stress in ex vivo cultured mouse hippocampal tissue slices. The present study provides deeper insights into plasma-mediated neuroprotection ultimately resulting in the development of novel therapies for a variety of neurological and, in particular, neurodegenerative diseases.
Highlights
Aging is associated with physical deterioration affecting every organ in the body, being the major risk factor for most neurodegenerative diseases (ND) [1]
The neurotoxic effects of Kainic acid (KA) were significantly reduced by the application of human plasma in cornu ammonis 1 (CA1), cornu ammonis 3 (CA3), and dentate gyrus (DG)
The application of human plasma without KA treatment led to a slight increase in cell death which was not significant compared to the untreated control
Summary
Aging is associated with physical deterioration affecting every organ in the body, being the major risk factor for most neurodegenerative diseases (ND) [1]. ROS are frequently produced in the brain, due to its high amount of mitochondria and its elevated oxygen and glucose consumption [12], which makes it on the other hand highly susceptible to ROS-mediated cellular damage via lipid peroxidation during aging [13] In neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, or cerebral ischemia, ROS can be generated through the excess release of excitatory neurotransmitters such as glutamate. In vivo studies confirmed the neuroprotective effect of fresh frozen plasma (FFP) after hemorrhagic shock (HS) and traumatic brain injury (TBI) by significantly reducing lesion size and swelling in the porcine system [31,32] Extending these promising observations, we investigated the effects of human plasma on oxidatively stressed ITSC-derived human neurons as well as on ex vivo mouse hippocampal slice cultures in the present study. Our observations may enable a future determination of the underlying molecular pathways driven by plasma and ameliorate plasma-based therapies against neurodegenerative diseases
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
