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. 2019 Dec 16;9:19162. doi: 10.1038/s41598-019-55631-8

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© The Author(s) 2019

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Heme modifies 20-day-old cortical organoid architecture by inducing early apoptosis and necrosis in its cells. Cortical organoids were treated with heme for 8 hours, and NRG-1 was then added for 18 hours. CPT treatment was used as a positive control for cell apoptosis. The results showed (A) that, compared to no treatment (a), heme induced the disorganization of cerebral organoid structure (b). NRG-1 improved the heme-induced lesion (c). CPT, used as a positive control for apoptosis, induced similar disorganization of cortical organoids (d). In addition, the apoptosis assay showed that heme increased cell necrosis in cortical organoids (B), while NRG-1 treatment reduced the injury. Representative images of cortical organoids (C) reinforcing the conclusion that heme had a toxic effect (b) compared to basal conditions, while NRG-1 had a protective role (d) compared to heme treatment (b). CPT also induced cell death compared to untreated condition (c) (a: p < 0.05 compared to basal conditions; b: p < 0.05 compared to heme treatment).