## 3 Discussion  
Chronic hyperglycemia in diabetic patients promotes the oxidation of glucose in mitochondria, which leads to the formation of excessive free radicals, thereby greatly increasing oxidative stress [28]. The glucotoxicity caused by hyperglycemia can decrease activity of antioxidant enzymes, including catalase, GPx, and SOD [29; 30; 31]; exacerbate oxidative stress; induce \(\beta\)-cell apoptosis and a gradual loss of \(\beta\)-cell mass and function, leading to insufficient insulin secretion; and result in diabetes [10; 32; 33]. Therefore, an approach to reduce the oxidative stress and apoptosis induced by glucotoxicity is a treatment strategy to reduce the risk of such pathological damage [16]. More and more studies have shown beneficial effects of many plant extracts or phytochemicals on the prevention and treatment of diabetes [3; 14; 15; 16; 17; 28]. Previously, SOE was demonstrated to have anti-inflammatory, \begin{table}
\begin{tabular}{c c c c} \hline \hline
**No.** & **Component** & \
\begin{tabular}{c} **Retention Time** \\ **(min)** \\ \end{tabular} &
\begin{tabular}{c} **Content** \\ **(mg/g Dry Extract)** \\ \end{tabular} \\ \hline
1 & Chlorogenic acid & 7.2 & 2.04 \(\pm\) 0.04 \\
2 & Syringic acid & 13.4 & 10.76 \(\pm\) 0.11 \\
3 & \(p\)-Coumaric acid & 24.4 & 0.70 \(\pm\) 0.03 \\
4 & Syringaldehyde & 25.4 & 0.39 \(\pm\) 0.02 \\
5 & Kirenol & 37.3 & 7.88 \(\pm\) 0.08 \\ \hline \hline \end{tabular}  
* The content of each component was estimated based on the standard curve constructed by the peak area of that reference compound at different concentrations. Data were estimated from three repeated experiments.  
\end{table} 
Table 1: Content of the main ingredients in SOE *. Figure 6: Main ingredients analysis of the SOE by HPLC. Peak 1: chlorogenic acid; peak 2: syringic acid; peak 3: \(p\)-coumaric acid; peak 4: syringaldehyde; and peak 5: kirenol. The analyses were performed by a Supelco C18 column, and a gradient of acetonitrile and 0.1% acetic acid was used as the mobile phase. The compounds were identified with those of reference compounds. antioxidant activity and can inhibit the activity of \(\alpha\)-glucosidase, pancreatic lipase and ACE and the formation of AGEs [19, 25]. This study investigated the effects of SOE on cell proliferation, intracellular ROS generation, activity of the antioxidant enzymes, and insulin secretion in HG-stimulated RN-m5f \(\beta\)-cells. Results in this study show that exposure of pancreatic \(\beta\)-cells in HG levels significantly reduced the cell viability (Figure 1A). When \(\beta\)-cells were treated with SOE alone, SOE promoted the growth of \(\beta\)-cells when the concentration was lower than 62.5 \(\mu\)g/mL but slightly inhibited the growth of \(\beta\)-cells when the concentration was higher than 250 \(\mu\)g/mL (Figure 1B). Under the induction of HG (50 or 100 mM glucose), SOE protected the growth of \(\beta\) cells (Figure 1C). Previously, it has been shown that SOE is cytotoxic to several human cancer cell lines (the IC\({}_{50}\) values were between 87.2 to 179.1 \(\mu\)g/mL), including RL-95 (endomettial cancer), A549 (lung cancer), HepG2 (hepatoma), FaDu (pharynx squamous cancer), MDA-MB-231 (breast cancer), and LNCaPP (prostate cancer). The action of SOE treatment was through arresting the cell growth (e.g., RL-95) in G2/M phase and induced cell apoptosis by up-regulating the expression of Bad, Bak, Bax, caspase-3, -8, and -9 and down-regulating the expression of Bcl-2 and Bcl-xL [23]. In spite of the fact that SOE exhibits cytotoxicity against cancer cells, results in our study demonstrate that SOE can provide a protective effect on the growth of pancreatic \(\beta\)-cells against HG-induced cytotoxicity. Glucotoxicity in \(\beta\)-cells can induce the production of excess ROS, which are free radicals generated from oxygen metabolism in mitochondria. Normal cells have an antioxidant defense system that can neutralize ROS and keep the cells at optimal redox potential to maintain normal cell functions [1, 34].