## 4 Discussion  
The gastric mucosa lining acts as a barrier against toxins such as Helicobacter infection, HCl in digestive juices, nonsteroidal anti-inflammatory agents, and alcohol [35]. Any cracks in this barrier can lead to gastric ulcers, gastritis, and even stomach cancer. If a rift occurs, the gastric acid secretion and accumulation of hydrochloric acid in the gastric mucosa are increased, the gastric mucosa itself is digested, and the gastric mucosa barrier breaks down [26,35]. Accordingly, a gastric mucosa protection effect is present if a substance suppresses or reduces in the HCl/EtOH-induced model gastric acid secretion [26]. Various fermentation processes enhance kiwi preservation, increase bioactive compound content, and increase the pharmacological activity of various antioxidant bases [36]. Lactic acid fermentation by bacteria can improve the bioavailability and the antioxidant and anti-inflammatory effects of the substance being fermented [37]. Fermentation of kiwi fruit puree powders produced using these bacteria is no exception. Gold kiwi was inoculated and fermented with two lactic acid bacteria, Lactococcus lactis VI-01 and Lactobacillus paracase VI-02, extracted, freeze-dried, and powdered for use in the study. As a result of analyzing the organic acid, total flavonoid, and carotenoid content of fermented gold kiwi (FGK) and general gold kiwi (GK), the active compounds of kiwi increased after fermentation (Table 3). In this study, three different doses of FGK (50, 125, and 250 mg/kg) were orally administered 1 h before the 150 mM HCl/60% EtOH solution treatment. The rats were measured for clinical symptoms after 30 min of HCl/EtOH solution treatment. After 1 h, changes in total hemorrhagic disease score, histopathology, and inflammatory markers were observed and all results were compared with 50 mg/kg of sucralate. HCl/EtOH-induced and pyloric ligation models are widely used to induce gastritis or gastric ulcers, as damage to the gastric mucosa and gastric wall can be observed by the unaided eye [38,39]. In the HCl/EtOH-induced gastric ulcer model, HCl causes severe damage to the gastric mucosa. Ethanol causes direct necrosis in the gastric mucosa and wall, resulting in a characteristic necrosis lesion due to reduced mucus formation and bicarbonate secretion [40]. Therefore, we adopted these two models to assess the gastric protective effects of FGK. Oral administration of FGK significantly reduced gastric lesions induced by HCl/EtOH and pyloric ligation. Rats treated with HCl/EtOH only showed a significant increase in redness and damage to the gastric mucosa (Figures 3-5). FGK administration significantly reduced gastric juice volume, pepsin activity, free acidity, and total acidity in pyloric ligation rats (Table 3). These results demonstrate that FGK improved gastritis and protected against gastric ulcers. Although the precise pathogenesis of gastritis has not been elucidated, the formation of reactive oxygen species (ROS) from ethanol has been shown to contribute to gastritis [40,41]. Excessive production of ROS causes oxidative stress, which causes various diseases [42,43]. A small amount of ROS generated in the stomach is quickly removed through the actions of various antioxidant enzymes and antioxidants. However, excess ROS can cause oxidative stress and damage to the gastric mucosa by overwhelming the antioxidant defenses [44,45]. Scavenging of free radicals plays a significant role in reducing or curing ulcers [46]. Kiwi