Fig 2: (A) Serum LCN2 level in the three groups. (B) Relative LCN2 mRNA levels in the hippocampal region in the three groups. (C) Relative LCN2 mRNA levels in different brain regions in the PSD group. (D) Relative LCN2 mRNA levels in different brain regions in the PS group. (E) Correlation of serum LCN2 level with the horizontal score of open field 2 weeks postoperation. (F) Correlation of serum LCN2 level with the self-grooming score of open field 3 weeks post operation. [#Compare with the PS group, P < 0.05, ##Compare with the PS group, P < 0.01; *Compare with the Sham group, P < 0.05, **Compare with the Sham group, P < 0.01; ▲▲Compare with post operation 1 week, P < 0.01; ∙Compare with post operation 2 weeks, P < 0.05, ∙∙Compare with post operation 2 weeks, P < 0.01; ⋄Compare with the right cerebral hemisphere, P < 0.05; △ Compare with the left cerebral hemisphere, P < 0.05, △ △ Compare with the Left cerebral Hemisphere, P < 0.01; Sham group (n = 6), PS group (n = 7), and PSD group (n = 10)].

Fig 3: Cisplatin-induced rise in kidney levels and histological indexes of renal tubular injury. Representative images for Western blots on total kidney lysates for kidney injury molecule 1 (KIM-1, (A)) and neutrophil gelatinase-associated lipocalin (NGAL, (B)) measured on day 3 after cisplatin (Cp, 20 mg/kg) or saline injections in male mice, homozygous (homo) and heterozygous (het) knockout for GPER1 gene, and wild-type (WT) littermates. Densitometric values (AU, arbitrary units) for kidney levels of KIM-1 (C) and NGAL (D) were normalized to the Ponceau S staining. Representative histological images of periodic acid-Schiff (PAS)-stained kidney sections from male homo, het, and WT mice on day 3 after Cp or saline injections are shown (E). Scale bar = 200 µm. Quantification using a semiquantitative scale (0–4) of indexes of renal injury is demonstrated (F). Data are presented as mean ± SEM (n = 7–13 mice/group). Statistical comparisons were performed by two-way ANOVA with Sidak’s post hoc test for multiple comparisons (C,D,F). p values for ANOVA and post hoc test results are displayed on the figures. AU, arbitrary units; Cp, cisplatin; Het: heterozygous knockout for GPER1 gene; Homo, homozygous knockout for GPER1 gene; KIM-1, kidney injury molecule 1; NGAL, neutrophil gelatinase-associated lipocalin; PAS, periodic acid Schiff; Sal, saline; WT, wild-type.

Fig 4: Tourniquet use leads to increased evidence of remote organ injury. Graphs show comparison of NGAL, Albumin, Wet:Dry Lung Ratio, HMGB1, Calprotectin, and TREM-1, between Blast Complex HLI 150 and Blast Complex Control from 6 h to POD 7 following injury. Graphs shown as mean and 95% CI with statistical testing using two-way ANOVA with Holm-Sidak correction for multiple paired comparisons where appropriate. Shaded horizontal band denotes the 95% CI of the mean serum concentrations of analytes in the naïve group. Significance shown as *p < 0.05; **p < 0.01; ***p < 0.001, ns not significant

Fig 5: (A) NO level in the supernatant of primary microglia. (B) Length of primary microglia. (C) Migration ability of primary microglia. (D) Phagocytic ability of primary microglia. (E) Uptake of 1 ml microspheres for 5 h by Con-MG. (F) Uptake of 1 ml microspheres for 5 h by LCN2-MG. (Primary microglia were identified by Iba1 expression (green), and nuclei were stained with DAPI (blue). Scale bars: 20 μm. [**Compare with Con-MG, P < 0.01. Con-MG (n = 3), LCN2-MG (n = 3)].