Fig. 4.

Ginsenoside CK reduces neuronal injury and mitochondrial damage in the I/R rat model. (A) After ginsenoside CK pretreatment (10 mg/kg/day, 500 μL, dissolved in ddH₂O) for 14 days prior to I/R injury, TTC staining was used to detect the ischemic area in rat brain tissues from the sham group (without insert the nylon monofilament), I/R group (middle cerebral artery occlusion), and I/R + CK group; the red represents the living neurons, and the white represents the damaged neurons. (B) The ischemic volume in rat brain tissues from (A) was analyzed by ImageJ software. (C) Longa neurological deficiency scale was used to analyze the neurological function of rats. (D) The water content of brain tissue was measured by dry and wet weight method. (E) H&E and Nissl staining were used to analyze the degree of neuronal damage; scale bar = 20 μm. (F) The expression of MAP2 in cerebral cortex was detected by immunofluorescence assay; DAPI was used for staining nuclei; scale bar = 50 μm. (G) Quantitative analysis of the mean fluorescence intensity of MAP2 from (F). (H) Live mitochondria from cerebral cortical neurons of different groups were extracted to measure OCR in basal respiration and under the mitochondrial stress with oligomycin and FCCP. (I) Enzyme activity of the mitochondrial complexes in rat brain tissues was examined by enzymatic kits. Data are shown as mean ± SEM, n = 5 per group; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, significantly different as indicated; one-way ANOVA followed by Tukey's post hoc test.