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Immunoregulatory and neuroprotective activity of ovocystatin
Published online by Cambridge University Press: 01 September 2022
Abstract
Ovocystatin has beneficial properties for cognitive function in young rats and might prevents aging-related cognitive impairment in older animals, as well as reduces memory decline in APP/PS1 mice model.
Our study aimed at assessing the impact of ovocystatin on microglia activation and neurogenesis.
Immunoactivation: Mouse wild type microglia were stimulated with ovocystatin at dose of 100 micrograms/ml. The effect of ovocystatin on nitric oxide production and interleukin 1 beta secretion were determined. Neurogenesis: Primary rat hippocampal neurons of H19-7 cell line was used. The impact of ovocystatin on proliferation, nitric oxide production, and expression of markers of neurogenesis: microtubule-associated protein 2 (MAP2, isoforms A/B and C/D) and Synapsin 1, were determined.
It was shown that ovocystatin does not stimulate microglial cells to produce inflammatory mediators. Whereas, no toxic effect of ovocystatin (1-100 ug/ml) on H19-7 cells viability, and dose-dependent down-regulation of proliferation were demonstrated. It was also shown that in primary hippocampal neurons of H19-7 cells incubated with ovocystatin (100 micrograms/ml), the expression level of MAP2 C/D (75kDa) - characteristic form of immature neurons is unchanged. However, the increased expression of MAP2 A/B protein (280 kDa) – characteristic for mature neurons was observed after 6 and 24h incubation with ovocystatin. Relatively to MAP2 A/B, increased expression of synapsin 1 was observed.
The ovocystatin might be a potential activator of molecular mechanisms in primary hippocampal neurons, participating in regulation of neurogenesis. Nevertheless, further studies are needed.
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- Information
- European Psychiatry , Volume 65 , Special Issue S1: Abstracts of the 30th European Congress of Psychiatry , June 2022 , pp. S700
- Creative Commons
- This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
- Copyright
- © The Author(s), 2022. Published by Cambridge University Press on behalf of the European Psychiatric Association
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