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. 2020 Aug 5;57(11):4563–4577. doi: 10.1007/s12035-020-02045-7

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — a Anti-oxidative effects of 50 μM perforin inhibitor (PFI) and its LAT1-utilizing prodrug (PFI-PD) as well as α-tocopherol (Toco; vitamin E) on lipopolysaccharide (LPS)-induced lipid peroxidation in primary astrocytes after 24 h incubation (in vitro). b Anti-oxidative effects of 30 μmol/kg of perforin inhibitor (PFI) (dark gray bars) and its LAT1-utilizing prodrug (PFI-PD) (light gray bars) after lipopolysaccharide (LPS)-induced neuroinflammation (with 250 μg/kg dose per day for 3 consecutive days) in mice (in vivo). The studied compounds were given to mice as a curative treatment only on the 3rd and 4th days of the experiment or as a preventative treatment for 4 days together with LPS. Oxidative stress was measured as malondialdehyde (MDA) formation in the astrocytes (normalized to protein content in a) or in the brain (normalized to tissue weight in b). The data are presented as mean ± SD (n = 3–4). An asterisk denotes a statistically significant difference from the respective LPS or control group (* P < 0.05, ** P < 0.01, *** P < 0.001, one-way ANOVA, followed by Tukey’s test)