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Fig. 4 | Fluids and Barriers of the CNS

Fig. 4

From: Long-term administration of CU06-1004 ameliorates cerebrovascular aging and BBB injury in aging mouse model

Fig. 4

The effect of long-term CU06-1004 administration on cerebrovascular aging in mice. A Whole-mount view of brains from 6-week-old (young), 24-month-old vehicle-treated (old-veh), and 24-month-old CU06-1004–treated mice (old-1004) B, C Quantification of maximal brain diameter (B) and brain-to-body weight ratio (C, brain index) in young (n = 6), old-veh (n = 10–12), and old-1004 (n = 10–12) mice. D, E Representative images and quantification of capillary vessel density in the cortical and hippocampal regions of young, old-veh, and old-1004 mice. Scale bar = 50 µm. F Representative images of Senescence-associated β-galactosidase staining (SA-β-gal) in cortical regions of young, old-veh, and old-1004 mice (n = 7 per group). G Stained levels of SA β-gal-positive cells, digitized for analysis by Photoshop. Quantified SA-β-gal positive densities in vascular region was calculated as the ratio of the area covered by SA-β-gal positive vascular area to the total vascular area. And quantified SA-β-gal positive densities in non-vascular region was calculated as the ratio of the area covered by SA-β-gal positive non-vascular area to the total area excluding the vascular area. Interestingly, in the old-1004 group, SA-β-Gal+ cell prevalence was reduced in both vascular and non-vascular region, suggesting that CU06-1004 may alleviate cerebrovascular aging in both vascular and non-vascular cells (G). All data were analyzed with one-way analysis of variance, followed by Tukey’s multiple comparison test. ###P < 0.001 vs. young. *P < 0.05 vs. old-veh. Results are presented as the mean, and error bars represent the standard deviation

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