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. 2019 Aug 3;8(8):273. doi: 10.3390/antiox8080273

Figure 1.

Figure 1

Ginseng promotes the long-term recovery of permanent cerebral ischemic damage in an Nrf2-dependent manner. (A) Experimental design. All mice received 7 days of oral administration of ginseng (Gin) or Vehicle (Veh; 100mg/kg/d; once daily), and were then subject to pdMCAO. The last administration was performed at 2 h before pdMCAO. (B and C) At 28 days after pdMCAO, the effect of ginseng on ischemic brain lesion was determined by Cresyl violet staining. In the vehicle-pretreated groups, the Nrf2−/− mice displayed marked larger infarct volumes than the wildtype (WT) controls, supporting the critical role of Nrf2 in the long-term recovery of ischemic brain lesions. In contrast, the infarct volume was significantly reduced in ginseng-pretreated WT mice, but not Nrf2−/− mice, suggesting potential Nrf2-dependent neuroprotection by ginseng. ## p < 0.01, ∆ p < 0.05. WT-Veh: n = 7; WT-Gin: n = 12; Nrf2−/−-Veh: n = 7; Nrf2−/−-Gin: n = 11; pdMCAO: permanent distal middle cerebral artery occlusion; d: day; Gin: ginseng; Veh: vehicle; n.s.: no significance.