Baicalin’s Therapeutic Time Window of Neuroprotection during Transient Focal Cerebral Ischemia and Its Antioxidative Effects In Vitro and In Vivo

Figure 2

Therapeutic efficacy of baicalin in rats undergoing middle cerebral artery occlusion. (a) Flow chart of the determination of neurological function in injured rats at 24, 48, and 72 h after MCAO. (b) The neurological scores were determined in rats with MCAO (1.5 h) at various survival times after the onset of ischemia. Baicalin (15 mg/kg) or saline treatments were administered at 0 and 4 h after the onset of ischemia and after 24 h twice a day. The scores shown are presented as the means ± SEM. **𝑃<0.01, baicalin group is significantly different from the corresponding control group (𝑛=8 for each group). (c) A flow chart of the time window experiment of baicalin. (d) Seven coronal brain sections (2 mm thick) were selected for tetrazolium chloride staining. The red stain represents noninjured (normal) tissues; white represents the infarct region. (e) The infarct volume was quantified as a percentage of the total volume, with large infarcts corresponding to a more severe injury. (f) The neurological scores in rats after 1.5 h MCAO and 22.5 h reperfusion. Baicalin (15 mg/kg) treatments were first administered at 0, 2, 4, or 6 h after the onset of ischemia in the different groups, and saline was administered at 0 h in the ischemic group. In addition, 4 h after the first treatment, baicalin was administered again. ^ΔΔ𝑃<0.01, ischemic group versus sham; **𝑃<0.01,*𝑃<0.05, baicalin-treated groups versus ischemia group (𝑛=10 for each group).