# Rosemary Leaf Extract Inhibits Glycation, Breast Cancer Proliferation, and Diabetes Risks
## 3 Results and Discussion
### Effect of Rosemary Extract on Oxidative Stress in Diabetic Rats  
Reactive oxygen species (ROS) are produced during normal cellular metabolism [38]. They are highly reactive molecules and excessive amount of ROS can cause oxidative stress and damage cell structures [38]. Generally, the formation of ROS is regulated by an antioxidant system with an enzymatic-related antioxidant, such as superoxide dismutase (SOD), being involved [39]. Compared with the normal control (NC) (0.42 \(\pm\) 0.02 U/mL), the increased activity of SOD (0.54 \(\pm\) 0.04 U/mL) in the diabetes control (DC) could be induced by the accumulation of superoxide anions (Table 2). It is a defense mechanism that protects pancreatic \(\beta\)-cells from the adverse effect of increased superoxide production [40]. However, the SOD activity in the rosemary extract-treated diabetes group (DRE) (0.64 \(\pm\) 0.03 U/mL) was significantly higher than DC and NC (Table 2). This correlates with a study that pomergnate extracts had the ability to ameliorate oxidative stress in plasma STZ-NA-induced diabetic rats, as evidenced by the improved antioxidant enzymatic status [39].  
Lipid peroxidation in diabetic rats could generate toxic products, inactivating membrane bound enzymes and damaging cell proteins through the direct free radical attack or chemical modification by its end products, such as malondialdehydedehyde (MDA) [41]. Thus, as an important marker of lipid peroxidation, serum MDA significantly increased from 6.74 \(\pm\) 0.49 nmol/L in NC to 8.43 \(\pm\) 0.53 nmol/L in DC, due to the breakdown of hydrogen peroxide to generate hydroxyl radical. Nevertheless, it was reduced to 7.15 \(\pm\) 0.26 nmol/L in DRE (Table 2). The inhibitory ability of RE could contribute to the Fe2+ chelating and radicals scavenging capability of the extract, thus preventing the initiation of oxidative damage [42]. This is in accordance with [PERSON]'s study, which showed that a decrease was observed in MDA formation at the rates of 31.8%, 36.7%, and 50.3% by pure rosemarinic acid in a dose-dependent manner [43]. Additionally, [PERSON] has reported that ethanoic extracts of plant Alhagi mauroum ameliorated the oxidative stress by decreasing the MDA level [44].  
Due to lipid auto-oxidation, free radicals were formed disproportionately and antioxidant defenses were consumed, leading to cellular function disruption and oxidative damage to membranes [45]. The T-AOC could reflect overall cellular endogenous antioxidative capability [46]. The activities of T-AOC in DC (1.65 \(\pm\) 0.10 U/mL) was significantly lower in NC (2.19 \(\pm\) 1.44 U/mL), due to oxidative stress and inflammatory reaction (Table 2), while RE improved the serum T-AOC to 6.13 \(\pm\) 0.82 U/mL. As reported in the studies of [PERSON], phenolic compounds such as rosemarinic acid and caffe acid had the capability of scavenging free radicals [16]. Thus, the phenolics in RE could inhibit ROS and ameliorate the oxidative stress which helped to mediate the T-AOC activity in diabetic rats. Similar results have shown that various herbs such as Ilex paraguariensis and panax notoginseng were able to improve plasma T-AOC activity [47; 48].