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.

Fig 5: Malnourished animals produce a sustained IL1-β driven inflammatory response in ear skin following Leishmania donovani-infected sand fly bites.a Representative inflammatory infiltrate of live cells gated on CD11b+ myeloid skin cells, then neutrophils (Ly6C+Ly6G+) and monocytes (Ly6C+Ly6G−) at 24 h post-challenge. Number of CD11b+ cells, neutrophils, and inflammatory monocytes at 24 h (b) and 72 h (c) post-challenge. d Representative inflammatory infiltrate of neutrophils and inflammatory monocytes expressing IL1-β on CD11b+ cells at 24 h post-challenge. Number of CD11b+ cells, neutrophils, and monocytes expressing IL1-β at 24 h (e) and 72 h (f) post-challenge. g Heme oxygenase 1 (HO-1) expression in skin tissue lysate 72 h post-infected bites by Western blot. HSP90, loading control. h Log 2-fold change of HO-1 density relative to WN-unchallenged controls. All groups were first normalized against the HSP90 loading control from (g). WN well-nourished, MN Malnourished, SF sand fly, ND needle. Data are representative of two experiments, n = 5 animals per group, and each data point represents a pool of 2 ears per animal (a–f). g, h Western blots from three independent experiments, n = 5–10 pooled ears per group. Data shows the median with interquartile range (IQR) (b, c, e, f), and mean (h). p ≤ 0.05 was considered significant. +p ≤ 0.09, *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, and ****p ≤ 0.0001. Significance was calculated by pairwise comparison by linear contrast expression (b, c, e, f) and Dunn’s test (h). Refer to Supplementary Data 2 file for the full statistical analysis report. All experiments were blinded.