## 4 Discussion
\begin{table}
\begin{tabular}{c c c c c c} \hline \hline \multirow{2}{*}{**Groups**} & \multicolumn{2}{c}{**Gastric juice**} & \multirow{2}{*}{**pH**} & \multirow{2}{*}{**Free Acidity (\(\mu\)Eq/mL)**} & \multirow{2}{*}{**Total Acidity (\(\mu\)Eq/6 h)**} & \multirow{2}{*}{**Pepsin Activity** (U/mL)**} \\  & **Volume (mL/6 h)** & & & & \\ \hline Control & 10.13 \(\pm\) 1.22 a & 1.01 \(\pm\) 0.08 c & 157.50 \(\pm\) 0.40 b & 1599.20 \(\pm\) 23.05 a & 5.02 \(\pm\) 0.22 a \\ FGK 50 & 8.30 \(\pm\) 1.13 a & 1.09 \(\pm\) 0.11 b & 117.25 \(\pm\) 3.22 a & 991.38 \(\pm\) 39.97 ab & 4.51 \(\pm\) 0.10 b \\ FGK 125 & 6.63 \(\pm\) 1.02 b & 1.23 \(\pm\) 0.06 b & 108.50 \(\pm\) 1.76 ab & 722.63 \(\pm\) 17.16 b & 4.26 \(\pm\) 0.30 b \\ FGK 250 & 4.53 \(\pm\) 0.95 c & 1.60 \(\pm\) 0.23 a & 69.17 \(\pm\) 3.17 a & 332.75 \(\pm\) 21.74 b & 2.26 \(\pm\) 0.05 d \\ SC 50 & 5.63 \(\pm\) 0.51 c & 1.38 \(\pm\) 0.09 b & 97.00 \(\pm\) 3.60 ab & 558.32 \(\pm\) 26.08 b & 2.89 \(\pm\) 0.04 c \\ \hline \hline \end{tabular} Control, rats treated with HCl/EtOH; SC 50, rats treated with HCl/EtOH and verlate; fermented gold kiwi (FGK); rats treated with HCl/EtOH and PKK (50, 125, and 250 mg/kg). The results are expressed as mean \(\pm\) SEM, (N = 8). \({}^{\text{a-d}}\) Different labels were significantly different at \(p<0.05\) between the treatments, as determined by [PERSON]’s analysis.  
\end{table} 
Table 3: Effect of FGK extract on gastric secretions in pyloric ligation rats. fruit contains antioxidants such as ascorbic acid, carotenoids, lutein, and flavonoids that protect against oxidative stress by removing free radicals [47]. We demonstrated in this study that FGK showed intense radical scavenging activity in a dose-dependent manner, consistent with a previous study (Figure 1) [48]. This indicates that FGK can help to protect tissues from oxidative damage. Our study also evaluated that pre-treatment with FGK prevented inflammatory conditions induced by HCl/EtOH acute gastritis. Injection of HCl/EtOH induces mucosal damage to the stomach, recognizes the damage-associated molecular patterns, and causes the subsequent stimulation of inflammatory cytokines such as IL-6 and TNF-\(\alpha\)[49]. This activation of inflammatory cytokines appears as an activation of NF-\(\kappa\)B. When NF-\(\kappa\)B is activated in response to oxidative stress, it migrates into the nucleus and activates inflammatory factors and cytokines such as iNOS, COX-2, TNF-\(\alpha\), and IL-6 [30]. In addition, iNOS-derived NO and PGE2 synthesized by COX-2 play a pivotal role in acute and chronic gastric inflammation [31]. As expected, FGK treatment reduces the inflammatory response and prevents gastric mucosa protection at a similar level to the standard gastric ulcer treatment, sucralate. These inflammatory cytokines promote gastric mucosal damage and delay the healing of gastric ulcers and gastritis by downregulating the enzymatic antioxidant defenses of the gastric mucosa [50]. Our results confirmed that the levels of iNOS, COX-2 overexpressed by gastritis induction, and increased TNF-\(\alpha\) and IL-6 were adjusted from FGK 250 levels to levels similar to the Control groups. PGE2, which is strongly associated with gastritis, has been reported to play a role in gastric homeostasis by regulating blood circulation and the epithelial cell motility of the gastric mucosa and inhibiting gastric mucus and gastric acid secretion [51; 52]. Ethanol reduced the mucosa PGE concentration, and PGE2 is the most abundant gastrointestinal prostaglandin, regulating its function in internal organs, including motility and secretion [52]. For this reason, PGE2 is commonly used as a biomarker to evaluate the preventive effects of various compounds on gastritis [53; 54]. In this study, the gastric protective effect of FGK was confirmed by observing the increased production of PGE2 in the gastric mucosa, suggesting that PGE2 partially mediates the gastric protective effect of FGK.