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Information × Registration Number 0218U007820, 0118U001374 , R & D reports Title Alterations of the cannabinoid/prostaglandin D2 receptor expression and pro-/anti-inflammatory cytokine profile under LPS-induced systemic inflammation: the action of N-stearoylethanolamine as a potent modulator of pro-inflammation response. popup.stage_title Head Kasatkina Ludmila Oleksandrivna, Registration Date 20-12-2018 Organization A.V.Palladin Institute of Biochemistry of National Academy of Sciences popup.description2 Neuroinflammation is associated with distant neurodegenerative changes, accumulation of aggregates of beta-amyloid peptide, and plays a crucial role in the progression of a wide range of neurodegenerative diseases. Our studies showed a correlation between changes in calcium homeostasis in neurons and the production of reactive oxygen species under LPS-induced inflammation. Our data demonstrated that synaptic vesicles clustering increased, while their fusions reduced in the presence of amyloid beta-1-42 oligomers, which are formed at the later stages of progression of neuroinflammation. Thus, the generation of reactive oxygen species and the changes of the basal level of Ca2+ in neurons are factors that modulate nervous transmission in the early stages of neuroinflammation, while disruption of beta-amyloid peptide homeostasis at later stages can cause significant inhibition of fusion of synaptic vesicles with the plasma membrane of the nerve terminals. Using FACS analysis in the laboratory of the partner country, expression of prostaglandin CRTH2 (DP2) and cannabinoid (CB1, CB2) receptors in primary macrophages and acutely isolated neurons (prefrontal cortex and hippocampus) was evaluated. We found that NSE affects the expression of CB2 in the hippocampus and CB1 / 2 in the prefrontal cortex, which correlates with changes in the neurotransmitter balance in these areas of the brain. The production of transforming growth factor beta-1 (TGFbeta1) increased in the prefrontal cortex under LPS-induced inflammation, whereas in the group receiving NSE, the level of both TGF? and the anti-inflammatory cytokine IL-10 decreased. The results show that CB1 / 2 and its interaction with TGFbeta signaling may be the endogenous mechanisms of the early neuroprotective reaction caused by the inflammatory process. Product Description popup.authors Є.А. Гудзь І.О. Трикаш popup.nrat_date 2020-04-02 Close