## 3 Results and Discussion
### Gastroprotective effect of BSBHE:\(\beta\)-CD Inclusion Complexes  
The loss of crucial defense mechanisms, such as a reduction in the activity of antioxidant enzymes, the destruction of the gastric mucus barrier, the production of reactive oxygen species (ROSs), which causes oxidative stress, and the activation of the innate immune system, are characteristics of the gastric lesion caused by ethanol [94]. In the present study, gastric ulcers were induced in mice to assess the gastroprotective effect of BSBHE:\(\beta\)-CD inclusion complexes (Figure 6). The administration of oral ethanol (96%, 0.2 mL/animal) to mice treated with saline (negative control) caused severe damage to the gastric mucosa, clearly producing the expected characteristic zone of necrotizing lesions of the mucosa, generally parallel along the stomach body axis (Figure 6A). As marked in Figure 6A, the lesions can be seen by the white arrows that point to formed stretches. BSBHE (Figure 6B), BSBHE:\(\beta\)-CD (Figure 6C), and carbonoxolone (Figure 6D) decreased the effect of stretch marks, suggesting the gastroprotective effect. Figure 5: X-ray diffraction (XRD) of samples containing BSHE and \(\beta\)-CD. (**A**) \(\beta\)-cyclodextrintrim molecule, (**B**) bacuri seed hexane extract (BSHE), (**C**) physical mixture between BSHE:\(\beta\)-CD, and (**D**) BSHE:\(\beta\)-CD inclusion complexes. Figure 7 shows the analysis of gastoprotective activity BSHE:\(\beta\)-CD inclusion complexes in gastric lesions induced by absolute ethanol in mice. Through the lesion area analysis, it can be confirmed that both BSHE and BSHE:\(\beta\)-CD show gastoprotective activity in this assay (Figure 7). The gastric lesion observed in the control group (saline) was 26.70 mm\({}^{2}\) (\(\pm\)2.56) of the mucosa area. When compared with the negative control, the animals treated with BSHE and BSHE:\(\beta\)-CD inclusion complex showed a significant reduction in the area of gastric lesions. BSHE at doses of 25 and 50 mg/kg reduced lesion area to 10.50 mm\({}^{2}\)\(\pm\) 2.48 (60.70%) and 8.72 mm\({}^{2}\)\(\pm\) 1.68 (67.40%), respectively; for BSHE:\(\beta\)-CD, the same doses reduced it to 8.53 mm\({}^{2}\)\(\pm\) 1.55 (68.10%) and 9.6 mm\({}^{2}\)\(\pm\) 1.10 (64.10%), respectively, showing significant lesion area reduction compared with the negative control, but without significance between them. The BSHE:\(\beta\)-CD inclusion complex at a dose of 100 mg/kg had the same effect as carbenoxolone and was more effective than BSHE (Figure 7). Animals treated with carbenoxolone (positive control) at a dose of 100 mg/kg had a decrease in ulcerative lesions of 2.34 mm\({}^{2}\), promoting 91.20% inhibition of the ulcerative lesion. The animals treated with BSHE:\(\beta\)-CD inclusion complexes at a dose of 100 mg/kg had a decrease in ulcerative lesions of around 89.5% (area equivalent to 2.8 mm\({}^{2}\)) when compared with carbenoxolone. These results justify the complexation to obtain better effects of a possible phytomediation obtained from the extract of the seeds of _Platonia insignis_ since BSHE:\(\beta\)-CD inclusion complexes in the proportion of 100 mg/kg proved to be more effective than the EHSB. It should be noted that the BSHE:\(\beta\)-CD inclusion complexes are in the proportion of 3:7 (BSHE:\(\beta\)-CD), that is, only 30% of the pure BSHE. Figure 6: Injury area of the gastric mucosa of the stomachs in mice. (**A**) Negative control treated with saline, (**B**) BSHE administered in the proportion of 100 mg/kg, (**C**) BSHE:\(\beta\)-CD inclusion complexes in the proportion of 100 mg/kg, (**D**) positive control: carbenoxolone (100 mg/kg). (The white arrows signal the stretches). The presence of terpenes and flavonoids in the BSHE may justify the inhibitory activity on gastric ulceration [95,96]. Phenolic compounds have an antiulcerogenic effect related to cytoprotective activity [97]. The _Platonia insignis_ Mart. has a high content of flavonoids and sesquiterpenes [98, 99, 100].