GFAP Antibody - #DF6040

Fig. 5.| The expression of CD200 and CD200R was up-regulated induced by treadmill exercise after stroke in rats.The effect of treadmill exercise on the protein levels of CD200 and CD200R in the ischemic cortex (A-C) and hippocampus (D-F) at 7 and 28 days after tMCAO. CD200R staining shows protein expression at 7 and 28 days after treadmill exercise post-stroke (G). CD200R colocalizes with activated microglia (Iba1+cells, white arrows), not colocalizes with neural stem cells (Nestin+ cells) and astrocytes (GFAP+ cells), Scale bar: 50 μm. N = 4. Results are showed as means ± SEM. # P < 0.05, ## P < 0.01, ### P < 0.001 versus the Sham group. *P < 0.05, ** P < 0.01, *** P < 0.001 versus the tMCAO group.

Fig. 8 Effects of HRS treatment on protein expressions in septic rats 48 h after LPS challenge. A Representative images of protein expression levels by western blot analysis in each group. B–E Statistical representation of relative protein expressions of GFAP, IBA-1, BCL-2 and BAX; respectively. All data are presented as mean ± SD ****p < 0.0001, ***p < 0.001, **p < 0.005, *p < 0.05. HRS Hydrogen-rich saline, LPS Lipopolysaccharide, GFAP Glial fibrillary acidic protein, IBA-1 Ionised calcium binding adaptor molecule 1, BCL-2 B-cell lymphoma 2

Fig. 4. Effects of compounds on GFAP and Iba-1 expression in the LPS-induced astrocytes (C6, treated with 10 mg/mL of LPS) and microglia (BV2, treated with 1 mg/mL of LPS). A. Representative fluorescence microscopy images of GFAP immunostaining (Magnification  20). B. Representative fluorescence microscopy images of Iba-1 immunostaining (Magnification  40). C. Histograms show relative changes of GFAP expressed as mean ± SD of the three independent experiments (n ¼ 3). Ctrl. ¼ Control, LPS ¼ Lipopolysaccharide (10 mg/mL); 3, 13, 16 ¼ treatments by compounds 3, 13, 16 (20 mM) along with LPS (10 mg/mL). D. Histograms show relative changes of Iba-1 expressed as mean ± SD of the three independent experiments (n ¼ 3). All the data were analyzed using Image Pro Plus and expressed as a percent of LPS group values (fluorescence intensity). (#) Significant difference (##p < 0.01, ###p < 0.001) vs. control and (*) significant difference (*p < 0.05 and **p < 0.01) vs. LPS.

FIGURE 2 The location and expression of CTRP1 in the brain analyzed by immunofluorescence (n = 3). (A) The expression of CTRP1 in neuron in the cortex, NeuN was used to label neuron. CTRP1 expression was observed by fluorescence microscope and is shown by green fluorescence. NeuN expression is shown by red fluorescence. The nuclei were stained with DAPI and is shown by blue fluorescence. (B) The expression of CTRP1 in astroglia in the cortex. GFAP was used to label astroglia. CTRP1 expression is shown by red fluorescence. GFAP expression is shown by green fluorescence. (C) The expression of CTRP1 in microglia in the cortex. IBA1 was used to label microglia. CTRP1 expression is shown by green fluorescence. IBA1 expression is shown by red fluorescence. (D) The intensity of CTRP1 and NeuN in the cortex. The representative images were acquired under × 400 magnification, scale bars = 50 μm. ****p < 0.0001 vs. sham group.

FIGURE 2 Effects of AB4 treatment on inflammatory infiltration and protein levels of IL‐1β, GFAP, NLRP3 and caspase‐1 in the spinal cord of the control, CIA and CIA + AB4 groups. (A, B) Representative haematoxylin and eosin staining images (A) and quantitative analysis (B) of the spinal cord sections. Scale bar = 20 μm. (C) Representative immunofluorescence staining images of IL‐1β, GFAP, NLRP3, caspase‐1 and cleaved caspase‐1 in the spinal dorsal horn. Scale bar = 20 μm. (D) Quantitative analysis of the fluorescence intensity of IL‐1β, GFAP, NLRP3, caspase‐1 and cleaved caspase‐1. (E, F) Western blot analysis and quantitative grey value analysis of IL‐1β, GFAP, NLRP3, caspase‐1 and cleaved caspase‐1 levels in the spinal cord of the control, CIA and CIA + AB4 groups. Data are presented as mean ± SD (n = 5). *p 

Fig. 6 |EPO benefit antiinflammation and axonal regeneration can be neutralized by ERK inhibition, and activator can mimic the effect of EPO. a The axonal special protein GAP43 immunofluorescence staining and histogram at 14 days (magnification × 400). b–e The inflammatory marker proteins immunofluorescence staining and histograms at 14 days, including CD86, GFAP, TNF-α, iNOS(magnification × 400). All data presented as mean ± SEM in each group. *p < 0.05 vs. SCI + saline group, **p < 0.01 vs. SCI + saline group. #p < 0.05 comparison between SCI + EPO group and SCI + EPO + PD98059, ##p < 0.01 comparison between SCI + EPO group and SCI + EPO + PD98059