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. 2022 Oct 26;19:262. doi: 10.1186/s12974-022-02626-4

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© The Author(s) 2022

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. 2 — Necroptotic morphology and overproduction of ROS in R28 cells induced by glutamate. a The typical morphological changes of necroptosis were detected in glutamate-treated R28 cells by transmission electron microscopy (TEM), including cell swelling, vesiculation of cytoplasmic organelles and rupture of the plasma membrane. Black arrows indicate mitochondria; white arrows indicate rupture of plasma membrane. b Representative phase-contrast and fluorescence microscope images of R28 cells incubated with the ROS probe DCFH-DA after exposure to glutamate for different durations. The green fluorescence intensity indicated the level of intracellular ROS. Scale bar = 50 μm. c Cellular GSH levels were measured at 24 h after glutamate treatment. CTL: the control group; Glu: glutamate. The results were recorded as mean ± SD from at least three independent experiments. **p < 0.01 versus control group