Ursolic Acid Protects Sodium Dodecyl Sulfate-Induced Drosophila Ulcerative Colitis Model by Inhibiting the JNK Signaling

Ursolic acid (UA) is a bioactive molecule widely distributed in various fruits and vegetables, which was reported to play a therapeutic role in ulcerative colitis (UC) induced by toxic chemicals. However, the underlying mechanism has not been well clarified in vivo. Here, using a Drosophila UC model induced by sodium dodecyl sulfate (SDS), we investigated the defensive effect of UA on intestinal damage. The results showed that UA could significantly protect Drosophila from the damage caused by SDS exposure. Further, UA alleviated the accumulation of reactive oxygen species (ROS) and malondialdehyde (MDA) induced by SDS and upregulated the activities of total superoxide dismutase (T-SOD) and catalase (CAT). Moreover, the proliferation and differentiation of intestine stem cells (ISCs) as well as the excessive activation of the c-Jun N-terminal kinase (JNK)-dependent JAK/STAT signaling pathway induced by SDS were restored by UA. In conclusion, UA prevents intestine injury from toxic compounds by reducing the JNK/JAK/STAT signaling pathway. UA may provide a theoretical basis for functional food or natural medicine development.

Automated summary

Ursolic acid (UA), a bioactive molecule found in fruits and vegetables, has therapeutic potential in ulcerative colitis (UC) induced by toxic chemicals. In this study, using a Drosophila UC model, the protective effect of UA on intestinal damage induced by sodium dodecyl sulfate (SDS) was investigated. The results showed that UA could protect against SDS-induced damage by reducing oxidative stress and restoring the activity of antioxidant enzymes. Additionally, UA inhibited the excessive activation of the JNK-dependent JAK/STAT signaling pathway. These findings suggest that UA has potential for the development of functional food or natural medicine for UC.