## 3 Results
### Effects of the SBE on Apoptosis in the Hippocampus of A\(\beta\) 1-42 Treated Mice  
To demonstrate the protective effect of SBE on A\(\beta\)-induced apoptosis, the protein expression levels of Bax, Bcl-2, caspase-9, and cleaved PARP were analyzed in the hippocampal tissue. A\(\beta\) treatment significantly increased the protein levels of Bax, cleaved Caspase-9, and cleaved PARP. Conversely, the Bcl-2 protein levels decreased in the A\(\beta\)-treated group. Bcl-2/Bax are known as important proteins related to apoptosis in the mitochondria. The Bax protein level was dose-dependently reduced with SBE treatment by 31% and 51%, and SBE 100 mg/kg (\(p<0.01\)) significantly increased the levels of Bcl-2 and Bcl-2/Bax by 1.41- and 2.87-fold, respectively, compared to the A\(\beta\)-treated group in Figure 6. SBE 30 mg/kg and 100 mg/kg significantly reduced the levels of cleaved caspase-9 by 61%, and 76%, respectively, and reduced cleaved PARP by 33% and, 74%, respectively, compared to the A\(\beta\) treatment group. Therefore, we confirmed that SBE exhibited a prominent neuro-protective effect.  
Figure 5: Effects of SBE on antioxidant protein expression levels in the hippocampus of memory-impaired mice. (**A**) The expression of superoxide dismutase 1 (SOD1), SOD2, and glutathione peroxidase-1 (GPx-1) were detected by Western blotting analysis. (**B**) The protein bands were quantified and calculated using the relevant software. Protein expression levels were normalized on \(\beta\)-actin level. The data are expressed as means \(\pm\) SEM of independent experiments (\(n=3\)). \(\#\)\(p<0.01\) vs. Control group; \(\$<0.05\) and \(\$\$<0.01\) vs. Control group; \(\texttt{``}\texttt{*}\)\(p<0.01\) vs. A\(\beta\) (1–42) group.  
Effects of the SBE on A\(\beta\) Accumulation and Hyper-Phosphorylation of Tau Proteins in Hippocampus of A\(\beta\) 1-42 Treated Mice  
The pathological hallmarks of AD include A\(\beta\) accumulation and tau hyper-phosphorylation. The hyper-phosphorylation of the tau protein, can contribute to neuronal degeneration. Using western blot analysis, we confirmed that the A\(\beta\) injection promoted A\(\beta\) accumulation in the mouse hippocampus (Figure 7). The administration of SBE 30 mg/kg (\(p<0.01\)) and 100 mg/kg (\(p<0.01\)) significantly reduced A\(\beta\) accumulation in the hippocampus against as the A\(\beta\) injection group by 22% and 53%, respectively (Figure 7B). Based on the protective effect of SBE on A\(\beta\) accumulation, we confirmed the effect of SBE on tau phosphorylation in A\(\beta\) treated mice. A\(\beta\) treatment increased the tau protein phosphorylation compared to the normal group, and treatment with SBE 30 mg/kg and 100 mg/kg significantly attenuated A\(\beta\) induced hyper-phosphorylation of tau by 69% and 71%, respectively, compared to the A\(\beta\) treatment group.  
Figure 6: Effects of SBE on apoptotic protein expression levels in the hippocampus of memory-impaired mice. (**A**) The expression of Bcl-2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), cleaved caspase-9 and cleaved poly (adenosine diphosphate (ADP)-ribose) polymerase (PARP) was detected by Western blotting analysis. (**B**) The protein bands were quantified and calculated using the software. Protein expression levels were normalized on \(\beta\)-actin level. The data are expressed as means \(\pm\) SEM of independent experiments (\(n=3\)). ## \(p<0.01\) vs. Control group; $ \(<0.05\) and $\(<0.01\) vs. Control group; **\(p<0.01\) vs. A\(\beta\) (1–42) group.