Fig 1: DC32 activated the Nrf2/HO-1 pathway in CIA mice and the LPS-induced inflammatory model in NIH-3T3 cells. (A,B) The concentration of HO-1 in serum was measured by ELISA (n = 3). The Nrf2 and Keap1 in hind paw homogenates were analyzed by western blotting. DC32 (12.5, 25, 50 mg/kg) significantly increased the level of HO-1 and Nrf2 and reduced the expression of Keap1 in the hind paws (n = 3–4). The results are expressed as the mean ± SEM of three experiments, #P < 0.05 vs. the Sham group; *P < 0.05, **P < 0.01, ***P < 0.001 vs. the Model group. (C,D) The Nrf2, Keap1 and HO-1 protein levels and mRNA expression (24 h) were measured by western blotting (n = 4) and qPCR (n = 5) in vitro. DC32 increased the expression and transcription of Nrf2 and HO-1, and reduced the level of Keap1 without influencing its transcription. The results are expressed as the mean ± SEM and analyzed by one-way analysis of variance (ANOVA) and two-way ANOVA followed by Bonferroni's post-hoc tests, *P < 0.05, **P < 0.01, ***P < 0.001 vs. the LPS group.
Fig 2: Ttherapeutic efficiency of Cu5.4O USNPs on AKI mice.a Schematic illustration of the establishment and treatment schedule of AKI mice. b Survival curves of AKI mice with different treatment. c Weight variation of AKI mice at 24 h after treatment with Cu5.4O USNPs. Serum levels of d CRE and e BUN in AKI mice at 24 h after different treatment. f H&E staining of kidney tissues from each group. Triangles indicate the formation of casts. g Dihydroethidium (red fluorescence) and DAPI (blue fluorescence) staining of kidney tissues from each group. h SOD, i KIM-1, and j HO-1 levels measured in renal tissue homogenates from each group. In c–e and h–j, data represent means ± s.d. from four independent replicates (***P < 0.001; n.s., no significance, One-way ANOVA). Source data are provided as a Source Data file.
Fig 3: EUC’s effects on SAH-induced oxidative stress. EUC was dissolved into corn oil, and then the intraperitoneal injection (100 mg/kg) was performed 1 h before SAH and 30 min after SAH, respectively. (A–C) The MDA content, SOD and GSH-Px activity in brain tissues in rats of each group was determined (n = 3); (D–E) Western blot analysis was employed to detect the protein expression of HO-1 and Nrf2 in brain tissue of the rats of each group (n = 3). *p < 0.05, **p < 0.01 and ***p < 0.001.
Fig 4: Mechanisms of DC32-induced Nrf2 activation. DC32 induced autophagy by inhibiting Akt/mTOR and ERK activation. DC32 also increased the mRNA level and nuclear translocation of Nrf2 at the same time and then promoted p62 transcription and expression. The degradation of Keap1 via the autolysosome was then facilitated by p62. The Nrf2-p62-Keap1 feedback loop was subsequently triggered and further amplified the activation of Nrf2/HO-1.
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