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. 2021 Apr 15;27:39. doi: 10.1186/s10020-021-00299-y

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© The Author(s) 2021

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/.

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Fig. 1 — LncRNA-Fendrr and NLRC4-mediated inflammation is activated in the brain tissues of diabetic cerebral ischemia/reperfusion injury mice. The model of cerebral ischemia/reperfusion (I/R) injury in mice was established, and mice were divided into the DM-I/R group and the DM-sham group (control), n = 10/group. a HE staining was used to detect pathological changes in mouse brain tissue. Scale bar in the top line is 50 μm, and the bottom line is 20 μm. b TUNEL staining was used to detect neuronal apoptosis in mouse brain tissue. Scale bar in the top line is 50 μm, and the bottom line is 20 μm. c The expression of lncRNA-Fendrr was detected by qRT-PCR. d NLRC4, ASC, cleaved caspase-1 and IL-1β protein levels were detected by Western blotting. e The levels of IL-1β and IL-18 in brain tissue homogenate were detected by ELISA. f Detecting microglia markers Iba-1 and caspase-1 in the brain tissue of mice by Immunofluorescence (n = 3/group). Data are presented as means ± SD. P values were analyzed by Student’s t-test. **P < 0.01 and ***P < 0.001 versus the DM-sham group