Fig. 1. (a) Two-millimeter thick, TTC stained coronal sections of brains from rats subjected to transient occlusion of the middle cerebral artery for 1 h followed by 48 h of reperfusion. The highlighted non-stained core area is white, which is surrounded by a pink penumbra in the cortex, and a smaller penumbra area is also identified within the striatal region. The viable brain tissue is red in the figure. (b) Representative photographs representing HE staining of the cerebral cortex and the striatal region. Note: many neurons become pyknotic and deep-stained around the infarcts (b2) and no evident cell damage is present in the cerebral cortex and striatal region (b1). (c) Representative photographs representing Nissl staining of the cerebral cortex and the striatal region. There are a reduced number of neurons in ischemia-reperfusion side (c2) as compared with the no ischemia-reperfusion side (c1). Neurons were counted in the caudate-putamen area under microscope (40 × 10). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)

Fig. 2. Changes of immunohistochemical staining against BCL-2 in the neuronal cells of the caudate-putamen area after 1 h followed by 48 h of reperfusion. Panels show sham group (a), VD group (b), ginsenoside Rg₂ (2.5 mg/kg) group (c), ginsenoside Rg₂ (5 mg/kg) group (d), ginsenoside Rg₂ (10 mg/kg) group (e) and nimodipine group (50 ug/kg) (f). The positive number of BCL-2 cells in the VD group was decreased compared with sham group. The positive number of BCL-2 cells was significantly increased in the ginsenosides Rg₂ and nimodipine treatment groups. Moreover, cells of the ginsenoside Rg₂ (2.5 mg/kg) group (c) was lower than that of nimodipine group (f) and the ginsenosides Rg₂ (5 mg/kg) (d) and (10 mg/kg) groups (e) were higher than that of nimodipine group (f). Neurons were counted under microscope (40 × 10) and five different visual field was counted.

Fig. 3. Changes of immunohistochemical staining against HSP70 in the neuronal cells of the caudate-putamen area after 1 h followed by 48 h of reperfusion. Panels show sham group brain (a), VD group (b), ginsenoside Rg₂ (2.5 mg/kg) group brain (c), ginsenoside Rg₂ (5 mg/kg) group brain (d), ginsenoside Rg₂ (10 mg/kg) group brain (e) and nimodipine group (50 μg/kg) brain (f). The positive number of HSP70 cells in the VD group was decreased compared with sham group. The positive number of HSP70 cells was significantly increased in the ginsenosides Rg₂ and nimodipine treatment group. Moreover, cells of the ginsenosides Rg₂ (2.5 mg/kg) group (c) was lower than that of nimodipine group (f) and ginsenosides Rg₂ (5 mg/kg) (d) and (10 mg/kg) group (e) were higher than that of nimodipine group (f). Neurons were counted under microscope (40 × 10) and five different visual field was counted.

Fig. 4. Changes of immunohistochemical staining against BAX in the neuronal cells of the caudate-putamen area after 1 h followed by 48 h of reperfusion. Panels show sham group brain (a), VD group (b), ginsenoside Rg₂ (2.5 mg/kg) group brain (c), ginsenoside Rg₂ (5 mg/kg) group brain (d), ginsenoside Rg₂ (10 mg/kg) group brain (e) and nimodipine (50 μg/kg) group brain (f). The positive number of BAX cells in the VD group was increased compared with sham group. The positive number of BAX cells was significantly decreased in the ginsenosides Rg₂ and nimodipine treatment group. No significant change of the number of BAX positive cells was seen when ginsenosides Rg₂ (5 mg/kg) group (d) compared with the nimodipine group (f). The positive number of BAX cells in ginsenosides Rg₂ (2.5 mg/kg) and ginsenosides Rg₂ (10 mg/kg) group changed significantly when compared with nimodipine group (f). Neurons were counted under microscope (40 × 10) and five different visual field was counted.

Fig. 5. Changes of immunohistochemical staining against P53 in the neuronal cells of the caudate-putamen area after 1 h followed by 48 h of reperfusion. Panels show sham group brain (a), VD group (b), ginsenoside Rg₂ (2.5 mg/kg) group brain (c), ginsenoside Rg₂ (5 mg/kg) group brain (d), ginsenoside Rg₂ (10 mg/kg) group brain (e) and nimodipine (50 μg/kg) group brain (f). The positive number of P53 cells in the VD group was increased compared with sham group. The positive number of P53 cells was significantly decreased in the ginsenosides Rg₂ and nimodipine treatment group. No significant change of the number of P53 positive cells was seen when ginsenosides Rg₂ (5 mg/kg) group (d) compared with the nimodipine group (f). The positive number of P53 cells in ginsenosides Rg₂ (2.5 mg/kg) and ginsenosides Rg₂ (10 mg/kg) group changed significantly when compared with nimodipine group (f). Neurons were counted under microscope (40 × 10) and five different visual field was counted.

Effects of ginsenosides Rg₂ on neurological responses and memory performance in rats subjected to MCAO-reperfusion

N = 8. Data represent mean ± S.D.

Effects of ginsenoside Rg₂ on BCL-2, HSP70 positive neuronal numbers of the caudate-putamen in rats subjected to MCAO-reperfusion

N = 8. Data represent mean ± S.D.

Effects of ginsenoside Rg₂ on BAX, P53 positive neuronal numbers of the caudate-putamen in rats subjected to MCAO-reperfusion

N = 8. Data represent mean ± S.D.