## 3 Results
### Brainon Upregulates the Expression of SOD-1 and SOD-2 in SCO-Induced Hippocampal Tissue  
To examine the effects of Brainon on antioxidant enzymes, we determined SOD-1 and SOD-2 levels in SCO-treated hippocampal tissue of mice. SCO treatment significantly decreased SOD-1 and SOD-2 levels in comparison with that in the Normal group. However, administration with 30 (\(p<0.01\)) and 100 (\(p<0.01\)) mg/kg Brainon increased SOD-1 levels by 1.6- and 3.6-fold, respectively, whereas administration with 50 mg/kg (\(p<0.01\)) of GBE recovered the decreased SOD-1 levels 3.9-fold with SCO treatment. Furthermore, treatment with 100 mg/kg (\(p<0.01\)) Brainon and 50 mg/kg (\(p<0.01\)) GBE also enhanced SOD-2 levels by 1.9- and 2.1-fold, respectively, in comparison with the mice in the SCO-injected group (Figure 6).  
Figure 4: Effects of Brainon on acetylcholinesterasecholinesteraseerase (AChE) activity and acetylcholine (ACh) level in mice hippocampal tissues. The hippocampal tissues were homogenized, and the supernatant was used for calculation of (**A**) AChE activity and (**B**) ACh level. Values were calculated in units per mg protein are represented as means \(\pm\) SEM (\(n=3\)). ## \(p<0.01\) vs. Normal group; * \(p<0.05\) and ** \(p<0.01\) vs. SCO-treated group.  
Brainon Decreases Interleukin(IL)-1\(\beta\), IL-6, and Tumor Necrosis Factor (TNF)-\(\alpha\) mRNA Expression in SCO-Induced Hippocampal Tissue  
The effects of Brainon on the expression of IL-1\(\beta\), IL-6, and TNF-\(\alpha\) mRNA in the hippocampal of SCO-treated mice were confirmed using real-time qPCR (Figure 7). SCO treatment significantly increased expression of IL-1\(\beta\), IL-6, and TNF-\(\alpha\) mRNA compared to that in the Normal group (\(p<0.01\)). Figure 7 shows that the expression of IL-1\(\beta\) mRNA significantly decreased after treatment with 100 mg/kg Brainion (\(p<0.01\)) and 50 mg/kg GBE (\(p<0.01\)) by 30% and 18%, respectively, compared to the SCO-injected group. In comparison with the SCO-injected group, expression of IL-6 mRNA was reduced dose dependently after treatment with 30 (\(p<0.05\)) and 100 (\(p<0.01\)) mg/kg Brainion by 25% and 29%, respectively, and even further reduced by 35% after treatment with 50 (\(p<0.01\)) mg/kg GBE. Treatment with 100 mg/kg Brainion (\(p<0.01\)) and 50 mg/kg GBE (\(p<0.01\)) considerably alleviated TNF-\(\alpha\) mRNA expression by 22% and 28%, respectively, compared to that in the SCO-injected group.  
Figure 5: Effects of Brainon on CREB-BDNF pathway in the memory deficit mice hippocampal tissues. (**A**) Brain-derived neurotrophic factor (BDNF) and phosphorylation of cAMP-response element-binding protein (CREB) was measured via western blotting. (**B**) The protein band density was determined using the software. Phosphorylation levels of the CREB protein were normalized using the CREB, and BDNF protein was normalized using the GAPDH. Values are expressed as means \(\pm\) SEM (\(n=3\)). ##\(p<0.01\) vs. Normal group; *\(p<0.01\) vs. SCO-treated group.  
Figure 6: Effects of Brainon on anti-oxidant related protein levels in the hippocampal tissues of memory deficit mice. (**A**) Superoxide dismutase (SOD)-1, and SOD-2 protein expression were evaluated via western blotting. (**B**) The protein band density was measured utilizing by the software. Protein was normalized using the GAPDH. Values are represented as means \(\pm\) SEM (\(n=3\)). ##\(p<0.01\) vs. Normal group; *\(p<0.01\) vs. SCO-treated group.