AIF1/IBA1 Antibody - #DF6442

Fig. 3. HXP reduced neuroinflammation in MCAO rats by promoting MCPIP1-mediated microglia M2 polarization. A. After reperfusion for 7 d, brain water contents were examined. B. Brain infract volume was detected by 2,3,5-Triphentltetrazolium chloride staining. C. Changes in IL-1β, IL-6, iNOS, and TNF-α were measured via ELISA assy. D. Representative images of histopathological analysis. Scale bar, 20 µm. E. Representative immunofluorescence staining for CD206 (red) and Iba1 (green) in brain tissues. Scale bar, 20 µm. F. The expression of MCPIP1, CD16, iNOS, CD206, Arg1, and PPARγ was detected using Western blotting assay. Data are represented as mean ± standard deviation (N = 5). * * P 

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

Figure 8. CBDV inhibits chronic morphine treatment-induced glial activation and pro-inflammatory factors IL-6 and TNF-α mRNA expression in NAc. (A–C) Representative double immunofluorescent staining images of Iba1 and GFAP for the control group (A), morphine group (B), and morphine + CBDV group (C). NAc regions were collected following the final behavioral testing shown in Figure 7B . (D, F) The quantification of microglia (D) and astrocytes (F). (E, G) The size of the microglia (E) and astrocytes (G). (H, I) Total RNAs were extracted and qRT-PCR was performed to measure the expression of TNF-α (H) and IL-6 (I) in NAc. Scale bar: 200 μm. All the data represented mean ± S.E.M. ## P < 0.01, ### P < 0.001 versus the control group; *P < 0.05, **P < 0.01, ***P < 0.001 versus the morphine group.

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 1 The expression of microglia and amyloid‐β (Aβ) plaques in wild‐type (WT) and Alzheimer's disease (AD) mice brains. (A) The distribution of microglia and Aβ plaques in mice brains. (a1, b1) Visual cortex, (a2, b2) auditory cortex, (a3, b3) pear‐shaped cortex, (a4, b4) DG, (a5, b5) CA1, (a6, b6) CA2, (a7, b7) CA3, (a8, b8) amygdala, and (a9, b9) hypothalamus. Iba1 (red) for microglia, 4G8 (green) for Aβ, DAPI (blue) for nuclei. Scale bar: a–b, 500 μm; a1–a9, 100 μm; b1–b9, 100 μm. (B–E) The number and area ratio of microglia and Aβ plaques were detected. The results are presented as the mean values ± SEM, n = 4 per group.