ArticleJournal of anesthesia2018
Angiotensin II-mediated suppression of synaptic proteins in mouse hippocampal neuronal HT22 cell was inhibited by propofol: role of calcium signaling pathway.
Article in Journal of anesthesia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Effects of propofol on presynaptic synapsin phosphorylation in the mouse brain in vivo.Brain research · 2024Article
- Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons.Oxidative medicine and cellular longevity · 2022Article
- Upregulation of the P2X7 receptor promotes CaAmerican journal of translational research · 2021Article
- Canonical Wnt Signaling Modulates the Expression of Pre- and Postsynaptic Components in Different Temporal Patterns.Molecular neurobiology · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAngiotensin II (Ang II) has been shown to be involved in neurological disorders. Propofol demonstrated neuroprotective effects in neurons.
methodsMouse hippocampal HT22 cells were pre-treated with propofol, followed by Ang II treatment. The expression of synaptic proteins (synapsin I and PSD95) was examined. The effects of propofol on Ang II-induced NADPH oxidase expression and superoxide anion generation were examined. The effects of propofol on intracellular calcium concentration, the activation of calcium/calmodulin-dependent protein kinase II (CaMKII), and protein kinase C (PKC) were measured.
resultsAng II reduced the expression of synapsin I and PSD95, which was attenuated by propofol. Ang II-induced effects were blocked by Ang II type 1 receptor (AT1 receptor) blocker. Ang II induced the expression of NADPH oxidase and caused superoxide anion accumulation, which were attenuated by propofol. In addition, propofol induced intracellular calcium concentration, and activated CaMKII as well as PKCβ. Importantly, the Ang II-mediated effects were diminished by α-tocopherol, and the propofol-mediated effects were alleviated by calcium chelator, CaMKII inhibitor, and PKCβ inhibitor.
conclusionAng II, via AT1 receptor, induced oxidative stress and reduced the expression of synapsin I and PSD95 in HT22 cells. Propofol may increase synapsin I and PSD95 expression by inhibiting oxidative stress and stimulating calcium signaling pathway.
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