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. 2022 Jun 1;13(3):943–959. doi: 10.14336/AD.2021.1029

Figure 5.

Figure 5.

Inhibiting C3d+/GFAP+ astrocytes formation reduced BBB disruption and gap formation of tight junction in tMCAO mice. (A) Photographs shows Evans blue (EB) exudation for the whole brain and brain sections in the semaglutide treated tMCAO mice, tMCAO mice, and control mice at 3 days after tMCAO. The value of extravasated EB was recorded by a spectrophotometer at 610 nm. Bar graph showed the quantitative analysis of Evans blue leakage in these 3 groups. Data are mean±SEM, n=3-5 per group. *p<0.05. (B) Photographs showed IgG staining in the coronal section of the brain following 3 days of tMCAO in the semaglutide treated tMCAO mice, tMCAO mice, and control mice. Scale bar=50 μm. Bar graph showed the mean IOD of IgG intensity in these 3 groups. Data are mean±SEM, n=6 per group. **p<0.01. (C) Photomicrographs showed CD31/claudin-5, CD31/ZO-1, and CD31/occludin double staining in the ischemic peri-focal areas in the semaglutide treated tMCAO mice, tMCAO mice, and control mice. White arrows indicated discontinuous labeling and gap formation. Scale bar=10 μm. Bar graph showed relative gap formation of ZO-1, claudin-5, and occludin. Data are mean±SEM, n=3 per group. *p<0.05, **p<0.01