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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: TREM-2-p38 MAPK signaling regulates neuroinflammation during chronic cerebral hypoperfusion combined with diabetes mellitus

Fig. 1

Models of DM and CCH were established in vivo and in vitro. a Schematic representation of the experimental protocol. All experiments were performed on the indicated weeks. (B-E) Detection of cerebral blood flow changes by LSCI. b The field of view (also known as the ROI) was 5 × 5 mm. c Representative contrast and photographic images of cerebral perfusion. d CBF absolute values at the following time points: baseline, immediately before BCCAO, immediately after BCCAO, and at 1, 2, 4, 8 weeks after BCCAO. Baseline refers to cerebral perfusion before occlusion. e Quantification of relative CBF in the ROIs (% of baseline for each animal). Values are expressed as the mean ± SEM (n = 3). *P < 0.05, CCH vs. Sham; #P < 0.05, DM CCH vs. DM. f, g Cell viability was determined using CCK-8 assay. Cell viability was decreased under hypoxia and hyperglycemia condition. f Cells were exposed to hypoxia (3%) for 24 h under normal glucose condition (5.5 mM). g Cells were exposed to different concentrations of glucose (5.5, 11.1, 16.7, or 33 mM) for 24 h prior to a 24 h normoxic (21% O2) or anaerobic (3% O2) incubation. Data are presented as the mean ± SEM from three independent experiments performed in triplicate. **P < 0.01; ***P < 0.001 compared with the control group

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