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. 2020 May 16;98(6):875–886. doi: 10.1007/s00109-020-01920-z

Fig. 1.

Fig. 1

CU06-1004 attenuates brain injury and the disruption of EC junctions after I/R.

Comparison of infarction volumes assessed by TTC staining in the sham, vehicle-I/R, and CU06-1004-I/R groups (a) and quantified (b). Evans blue extravasation from sham, vehicle-I/R, and CU06-1004-I/R groups (c) and the quantification of Evans blue in ipsilateral (d) and contralateral hemispheres (e). Neurological scores for sham, vehicle-I/R, and CU06-1004-I/R groups (f). Brain water content for sham, vehicle-I/R, and CU06–1004-I/R groups. Quantification of water content in the ipsilateral (g) and contralateral hemispheres (h). n = 5 per group. HBMECs were oxygen-glucose deprived for 6 h (i). After reoxygenation and treatment with vehicle or CU06-1004 (10 μg/mL) for 16 h, cells were stained with DAPI, ZO-1, and F-actin. Scale bars, 20 μm. *P < 0.05, **P < 0.01, and ***P < 0.001. Error bars indicate mean ± SEM. ns, not significant; Con, control; OGD/R, oxygen-glucose deprivation/reperfusion; DAPI, 4′,6-diamidino-2-phenylindole; ZO-1, zona occludens-1; F-actin, fibrous actin; 1004, CU06-1004