## 4 Discussion
\begin{table}
\begin{tabular}{c c c c} \hline \hline
**Animal Groups** & **MDA, umol/L** & **Catalase, mkat/L** & **GSH, umol/L** \\ \hline \multicolumn{4}{c}{Indomethacin gastropathy} \\ Non-treated control (H\({}_{2}\)O) & 6.5 \(\pm\) 0.39 & 17.2 \(\pm\) 0.94 & 926.2 \(\pm\) 36.47 \\ Negative control (Indomethacin + H\({}_{2}\)O) & 23.2 \(\pm\) 1.08 \(p\)\(\leq\) 0.01 ** & 10.4 \(\pm\) 0.74 & 584.7 \(\pm\) 38.06 \\ \multicolumn{4}{c}{\(p\)\(\leq\) 0.01 ** } \\ Experimental group I (Indomethacin + skimming, 1 mg/kg) & 9.5 \(\pm\) 0.50 \(p\)\(\leq\) 0.01 * & 13.8 \(\pm\) 0.61 & 805.7 \(\pm\) 66.60 \\ \multicolumn{4}{c}{\(p\)\(\leq\) 0.01 *} \\ Experimental group II (Indomethacin + skimming, 3 mg/kg) & 11.0 \(\pm\) 0.88 \(p\)\(\leq\) 0.01 * & 12.7 \(\pm\) 0.77 & 812.4 \(\pm\) 61.85 \\ \multicolumn{4}{c}{\(p\)\(\leq\) 0.01 *} \\ Experimental group III (Indomethacin + peucenidin, 16 mg/kg) & 12.3 \(\pm\) 1.15 \(p\)\(\leq\) 0.01 * & 12.9 \(\pm\) 0.42 & 832.4 \(\pm\) 66.63 \\ \multicolumn{4}{c}{\(p\)\(\leq\) 0.05 *} \\ Experimental group IV (Indomethacin + peucenidin, 48 mg/kg) & 13.3 \(\pm\) 0.89 \(p\)\(\leq\) 0.01 * & 13.9 \(\pm\) 0.42 & 906.1 \(\pm\) 53.92 \\ \multicolumn{4}{c}{\(p\)\(\leq\) 0.01 *} \\ Ethanol/steroid gastropathy & & & \\ Non-treated control (H\({}_{2}\)O) & 5.9 \(\pm\) 0.40 & 18.3 \(\pm\) 0.71 & 973.1 \(\pm\) 39.64 \\ Negative control (ethanol/prednisolone + H\({}_{2}\)O) & 20.2 \(\pm\) 0.95 & 10.3 \(\pm\) 0.63 & 671.7 \(\pm\) 66.60 \\ \multicolumn{4}{c}{\(p\)\(\leq\) 0.01 *} \\ Experimental group I (ethanol/prednisolone + skimming, 1 mg/kg) & 12.5 \(\pm\) 0.68 & 13.1 \(\pm\) 0.62 & 932.9 \(\pm\) 82.46 \\ \multicolumn{4}{c}{\(p\)\(\leq\) 0.01 *} \\ Experimental group II (ethanol/prednisolone + skimming, 3 mg/kg) & 14.1 \(\pm\) 0.70 \(p\)\(\leq\) 0.01 * & 12.8 \(\pm\) 0.41 & 845.9 \(\pm\) 56.30 \\ \multicolumn{4}{c}{\(p\)\(\leq\) 0.01 *} \\ Experimental group III (ethanol/prednisolone + peucenidin, 16 mg/kg) & 14.2 \(\pm\) 0.63 \(p\)\(\leq\) 0.01 * & 14.8 \(\pm\) 0.51 & 926.2 \(\pm\) 42.57 \\ \multicolumn{4}{c}{\(p\)\(\leq\) 0.01 *} \\ Experimental group IV (ethanol/prednisolone + peucenidin, 48 mg/kg) & 13.1 \(\pm\) 0.86 \(p\)\(\leq\) 0.01 * & 12.9 \(\pm\) 0.30 & 959.7 \(\pm\) 47.57 \\ \multicolumn{4}{c}{\(p\)\(\leq\) 0.01 *} \\ \hline \hline \end{tabular}  
*—vs. negative control group animals; **—vs. non-treated control group animals.  
\end{table} 
Table 4: Effect of coumarins on the state of pro- and antioxidant systems of Wistar rats, with indomethacin and ethanol/steroid gastropathy. Microcirculation disorders and hypoxic processes underlying the gastropathy pathogenesis contribute to the formation of reactive oxygen species and an increase in cell membrane lipid peroxidation processes. In addition, the improper functioning of antioxidant defense systems contributes to biological membrane damage and oxidative stress [82]. Our results show that _F. hystrix_ roots from the Baikal region are a rich source of coumarins, and most of them have not previously been described. The known data demonstrate that the Mongolian population of _F. hystrix_ accumulates various furocomarins (such as angelicin, columbianetin and its esters, oroselol, and vaginidiol and its esters [22]) that significantly differ from those of the Baikal population of _F. hystrix_, which contains glycosides and esters of umbelliferone, vaginidiol, and peucedanol. This difference may be associated with the climatic conditions that distinguish the Mongolian and Baikal regions. We found that coumarins from the _F. hystrix_ roots exhibit a gastoprotective effect with regard to indomethacin and ethanol/steroid gastropathy. The most pronounced gastoprotective effect, which helped to limit pronounced erosive-necrotic development in the gastric mucosa, was caused by skimmin at a dose of 1 mg/kg and peucenidin at doses of 16 and 48 mg/kg. The gastoprotective action of the studied individual compounds is attributed to their ability to inhibit lipid peroxidation processes and increase the antioxidant system activity.