Simvastatin–Ezetimibe enhances growth factor expression and attenuates neuron loss in the hippocampus in a model of intracerebral hemorrhage

Figures

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  Figure 1. Photomicrographs showing immunohistochemical staining (NeuN) of the rat hippocampal CA1 region at different magnification. The survival neurons with different intensity of NeuN staining in the hippocampal CA1.

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  Figure 2. Analyses of ICAM‐1 revealing no significant differences among the control, simvastatin, and combination therapy groups (a). The simvastatin group exhibited significantly elevated BDNF levels at all time points, while the combination therapy group exhibited significantly elevated BDNF levels at the 24‐h and 72‐h time points (b). *P < 0.05 for Bonferroni post hoc comparison vs. the simvastatin group; P < 0.05 for Bonferroni post hoc comparison vs. the combination group. Data are presented as means ± standard errors. ICAM‐1, intercellular adhesion molecule‐1; BDNF, brain‐derived neurotrophic factor.

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  Figure 3. The two therapy groups exhibited significant improvements in neurological function (a). *P < 0.05 for Bonferroni post hoc comparison vs. the control group. The Morris water maze test demonstrated better neurological functioning in the combination therapy group than in the control group (b). *P < 0.05 for the Bonferroni post hoc comparison vs. the combination therapy group.

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  Figure 4. There were no significant reductions in hematoma size in the control, simvastatin, or combination therapy groups (a). An analysis of perihematomal edema revealed that only the combination therapy group had significant reductions in perihematomal edema on day 7 after injury (b). T2 map image, black arrow indicating hematoma and red arrow indicating perihematomal edema (c). *P < 0.05.

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  Figure 5. Increased intracellular adhesion molecule‐1 expression was noted in the control group (no treatment), and greater brain‐derived neurotrophic factor (BDNF) expression was noted in the therapy groups relative to the control group.

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  Figure 6. Photomicrographs of immunohistochemical staining of rat hippocampal CA1 in the (a) combination therapy, (b) simvastatin, (c) control, and (d) sham groups using antibodies specific for NeuN. (e) Cell number mean ± SEM (via Aperio software analysis) indicating different staining intensities across groups. The survival neurons with different intensity of NeuN staining were demonstrated in Figure 1. *P < 0.05, **P < 0.01, ***P < 0.005 (Student’s t‐test).