Characterisation of the immunogenicity of stem cell derived neural cells in response to an inflammatory stimulus and flavonoid treatment
Cardiff Metropolitan University
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Neurodegenerative diseases (NDD) such as Alzheimer’s Disease (AD) and Parkinson’s disease (PD) are debilitating conditions characterised by the progressive degeneration of neurons within the central nervous system (CNS). These diseases currently have no known cure; however extensive research is being carried out into potential therapies to help alleviate or delay the onset of symptoms. Inflammation in the CNS is a common known pathology of both AD and PD respectively, and is modulated by different neural cells within the CNS. Furthermore, flavonoids are naturally occurring compounds found in plants and other food products, and have been widely researched for their anti- inflammatory properties in many models of disease. By looking at flavonoids mechanisms of neuroprotection, and by understanding the mechanisms of neuroinflammation it could be possible to find new novel treatments for NDD. The aim of this experiment is to characterise the immunogenicity of human embryonic stem cell (hESC) derived neural stem cells (NSC), astrocytes, and neurons in response to an inflammation induced by interferon gamma (IFN-γ). Furthermore, the anti- inflammatory effects of the flavonoid apigenin will be assessed by monitoring the expression of tumour necrosis factor alpha (TNF-α). The success of apigenin to modulate cytokine release could be of further use in treatments of chronic inflammatory conditions such as AD and PD. The current study tests the viability of NSCs, astrocytes and neurons to increasing concentrations of IFN-γ in order to gain an insight into the cell tolerance for this inflammatory cytokine. Moreover, an enzyme-linked immunosorbent assay (ELISA) was carried out to monitor the expression of TNF-α in response to inflammatory insult from IFN-γ, and further analyse the effects of adding the flavonoid apigenin. The results of the present study show that IFN-γ was unable to elicit a significant pro- inflammatory effect on NSCs, astrocytes and neurons viability, with potential questions left on the concentration-dependency of this effect. Furthermore, ELISA shows that again, IFNy did not increase the cellular expression of TNF-α, and apigenin did not show a significant ability to modulate the inflammatory cytokines present.
BSc (Hons) Biomedical Science
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