Fig 1.
Effects of CL218872 on hemorrhage, neurobehavioral function, and inflammatory response following ICH.
(A): Hemorrhagic area in the brain; (B): Neurobehavioral Deficit Scores (NDS) (n = 10 animals); (C): TNF-α (pg/mL) and IL-6 (pg/mL) concentrations in brain tissue homogenates measured by ELISA (n = 5 animals). (D-E): Protein expression levels of p65, phospho-p65 (p-p65), and TNF-α detected by Western blot analysis (n = 3 animals). Data are presented as mean ± SD. Statistical significance was determined by one-way ANOVA followed by Tukey’s post hoc test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001; ns, not significant.
Fig 2.
Histopathological evaluation of hippocampal regions in ICH mouse.
(A): H&E staining showing tissue morphology (Scale bars: 200 μm, 50 μm); (B): Nissl staining assessing neuronal integrity (Scale bars: 200 μm, 50 μm); (C): Golgi staining analyzing dendritic complexity (Scale bars: 250 μm, 50 μm). n = 5 animals per group.
Fig 3.
CL218872 reverses ICH-induced suppression of astrocyte activation in hippocampal regions.
(A): Representative immunofluorescence images of GFAP (green) and DAPI (blue) at 50 × magnification. Scale bar: 200 μm; (B): Quantification of GFAP across experimental groups. n = 5 animals per group. Statistical analysis by one-way ANOVA with Tukey’s post hoc test: *p < 0.05, **p < 0.01, ***p < 0.001.
Fig 4.
TEM of hippocampal synaptic ultrastructure in mice.
Magnification: 20,000 × ; Scale bars: 200 nm and 500 nm (n = 3 animals). M: mitochondria; SV: synaptic vesicles.
Fig 5.
CL218872 enhanced markers of synaptic reconstruction.
(A) Representative Western blots of BDNF, GAP-43, PSD95, and synaptophysin in Brain tissue. (B) Quantitative analysis of relative protein expression. Data presented as mean ± SD, n = 3 animals; *p < 0.05, **p < 0.01, ***p < 0.001.