# (-)-Fenchone Ameliorates TNBS-Induced Colitis
## 2 Results
### Effect of (-)-Fenchone in Intestinal Acute Inflammation in a TNBS-Induced Colitis Model
#### 2.2.1 Histological Analysis  
Histological sections of the colons belonging to the non-colitic, prednisolone, and (-)-fenchone groups stained with hematoxylin and eosin are shown in Figure 9A,C,D; the integrity of the mucosa (M) and goblet cells is observed. In the colitic group (5% tween 80) (9B), intense mucosal destruction is observed, with ulcer formation, which is characterized by organ surface necrosis, intense acute inflammatory reaction (*), and increased leukocyte infiltration. In sections stained with Masson's trichrome, it was found that (-)-fenchone (Figure 9H) reduced extracellular matrix deposition (\(p<0.001\)) 8.00 (5-14) compared to the colitic group (5% tween 80) who presented scar tissue (\(\infty\)) in the area of the mucosal ulcer 26.50 (20-30) (Figure 9F) (Figure 9).  
\begin{table}
\begin{tabular}{c c c c c} \hline \hline
**Groups** & **ULA (mm2)** & \begin{tabular}{c} **\% Lesion** \\ **Inhibition** \\ \end{tabular} & \
\begin{tabular}{c} **Lesion** \\ **Score** \\ \end{tabular} &
\begin{tabular}{c} **Weight/Length** \\ **(mg/cm)** \\ \end{tabular} \\ \hline Non-colitic & ND & ND & ND & 91.4 \(\pm\) 3.5 \\ Colitic (5\% tween 80) & 57.17 \(\pm\) 7.5 *** & 0 & 3.0 \(\pm\) 0.7 *** & 148.9 \(\pm\) 10.5 *** \\ Prednisolone & 11.00 \(\pm\) 2.1 *** & 81\% & 1.0 \(\pm\) 0.6 *** & 127.5 \(\pm\) 13.7 ** \\ (-)-fenchone & 11.50 \(\pm\)2.9 *** & 80\% & 1.5\(\pm\) 0.7 ** & 130.6 \(\pm\) 8.3 ** \\ (150 mg/kg) & & & & \\ \hline \hline \end{tabular} Data are expressed as mean \(\pm\) SD or median (minimum/maximum values). For parametric data, we used one-way ANOVA followed by [PERSON]’s and [PERSON]’s post-tests. For non-parametric data, we used the Kruskal-Wallis test and Dunn’s test. **_p_\(<\) 0.01, ***_p_\(<\) 0.001 compared to colitic groups; ***_p_\(<\) 0.001 compared to non-colitic group. (n = 7–10). ND = not detectable.  
\end{table}
Table 2: Effect of (-)-fenchone in sub-chronic phase with recurrence of the intestinal inflammatory process in a TNBS-induced colitis model.  
Figure 9: Microscopic effects of the colon of rats submitted to in sub-chronic phase with recurrence of the intestinal inflammatory process in a TNBS-induced colitis model and treated or not with (-)-fenchone. Representative photomicrographs of the animals’ colon from the experimental groups: HE staining: non-colitic (**A**), colitic (5% tween 80) (**B**), prednisolone 2 mg/kg (**C**) and (-)-fenchone 150 mg/kg (**D**). Masson trichrome: non-colitic (**E**), colitic (5% tween 80) (**F**), prednisolone 2 mg/kg (**G**), and (-)-fenchone 150 mg/kg (**H**). Colonic mucosa (M), acute inflammatory reaction (*), scarring tissue (\(\infty\)). Results are expressed as the median (minimum–maximum) of the parameters analyzed (n = 5, 3 sessions per animal). Kruskal–Wallis test and [PERSON]’s posterior test were performed using the software Graph Pad Prism 6. **_p_\(<\) 0.01 or ***_p_\(<\) 0.001 compared to the non-colitic group (5% tween 80).  
2.2 Effect of (-)-Fenchone in the Modulation of Antioxidant and Anti-Inflammatory Properties in Chronic Phase Colitis with Recurrence of the Intestinal Inflammatory Process GSH  
In determining the GSH, it was possible to verify that the colitic group (5% tween 80) showed a reduction in GSH levels to 39.8 \(\pm\) 4.3 nmol of GSH/mg protein compared to the normal group (59.6 \(\pm\) 5.7 nmol GSH/mg protein). However, administration of (-)-fenchone (150 mg/kg) to 53.5 \(\pm\) 6.3 nmol GSH/mg protein nearly restored baseline GSH levels (Figure 10A).