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. 2023 Feb 22;13(8):862–879. doi: 10.1016/j.jpha.2023.02.007

Fig. 3.

Fig. 3

Increased leukocyte infiltration and impaired tissue repair after glial scar disruption. (A) Representative fluorescent images of reactive astrocytes (glial fibrillary acidic protein (GFAP)) and infiltrated neutrophils (lymphocyte antigen 6 complex, locus g (Ly6g)) around the lesion at 7 days post-injury (dpi). (B) Quantification of infiltrated neutrophils into lesion border brain parenchyma at 3 dpi (n = 7/group). (C) Quantification of neutrophils that infiltrated into lesion border brain parenchyma at 7 dpi. ∗P < 0.05 vs. intracerebral hemorrhage (ICH) + control diet group (n = 7/group). (D) Quantification of lesion area surrounded by reactive astrocytes at 7 dpi. ∗∗P < 0.01 vs. ICH + control diet group (n = 6/group). (E) Quantification of lesion area surrounded by reactive astrocytes at 21 dpi. ∗∗P < 0.01 vs. ICH + control diet group (n = 6/group). (F) Representative fluorescent images of lesion area surrounded by reactive astrocytes (GFAP) at 7 and 21 dpi. (G) Representative fluorescent images of vessel (CD31) and astrocytes (GFAP, at juxtavascular and non-juxtavascular positions) around the lesion. (H) The proportion of juxtavascular and non-juxtavascular astrocytes. ∗∗P < 0.01 vs. juxtavascular group (n = 6/group). (I) Quantification of Evans blue extravasation at 7 dpi. ∗∗P < 0.01 vs. sham group, ∗∗∗P < 0.001 vs. sham group, and #P < 0.05 vs. ICH + control diet group (n = 3–9/group). (J) Quantification of chondroitin sulfate proteoglycan (CSPG)+ area at 7 dpi. ns: no significance (n = 5/group). DAPI: 4′,6-diamidino-2-phenylindole.