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. 2021 Sep 23;27:118. doi: 10.1186/s10020-021-00377-1

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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. 6 — Inhibiting autophagy abolished calcitriol (0.5 µg/kg)-induced Nrf2 activation following TBI in mice. a Representative images of Western blot staining for Keap1, cytoplasmic Nrf2, and nuclear Nrf2. b Statistical graphs of Keap1 protein expression. c Statistical graphs of expression of Nrf2 in the nucleus and cytoplasm. d, e Representative immunofluorescence images and statistical graphs of Nrf2 translocation (Bar = 50 µm). f The relative mRNA expression level of Nqo1. g The relative mRNA expression level of Gclc. h The relative mRNA expression level of HO1. i, j Representative images and statistical graphs of immunofluorescence assays of dihydroethidium (DHE) (Bar = 50 µm). Data are presented as means ± SEM (n = 5). *P < 0.05 and **P < 0.01 versus the indicated groups. (TBI: TBI model group; Calcitriol: TBI + calcitriol treatment group; CQ: TBI + calcitriol + CQ treatment group; Nrf2^−/−: TBI + calcitriol + Nrf2 knockout group)