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. 2020 Sep 11;17:269. doi: 10.1186/s12974-020-01941-y

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© The Author(s) 2020

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 10 — Extracellular cGMP normalizes the IL1β and HMGB1 in Purkinje cells of hyperammonemic rats. Immunohistochemistry was performed as indicated in methods with DAB staining using antibodies against IL1β (a) and HMGB1 (b). Representative images are shown. The content of IL1β (c) and HMGB1 (d) was quantified in Purkinje cells as described in the “Methods” section. Values are mean ± SEM of 6 rats per group. Values significantly different from control rats are indicated by asterisk and from hyperammonemic rats are indicated by “a”. *p < 0.05, **p < 0.01; a p < 0.05, aaaa p < 0.0001. Data were analyzed using a one-way analysis of variance (ANOVA) followed by Turkey post hoc