Reserpine Ameliorates 1,2-Dimethylhydrazine-induced Colon Cancer through Regulating Xenobiotic Enzymes and Bax/Caspases/Bcl-2-mediated Apoptotic Mechanisms in Rats

Background Colon cancer is a significant public health issue, known as a major cause of cancer-associated mortalities globally. Understanding the underlying molecular mechanisms that direct the onset of colon cancer is necessary to develop novel therapeutic targets. Objectives This study was dedicated to studying the anti-cancer properties of the reserpine against 1,2-dimethylhydrazine (DMH)-treated colon cancer in rats. Materials and Methods In the present work, colon cancer was triggered in rats by the administration of DMH and thereafter treated with reserpine prior to and throughout the DMH administration. After completing the treatments, alterations in body weight were assessed. The levels of inflammatory cytokines, oxidative markers, xenobiotic-metabolizing enzymes, tumor markers, and apoptotic proteins in the rats were carefully analyzed using commercial kits. The colon mucosa of the rats was subjected to histopathological studies. Results The current results proved that the administration of reserpine significantly increased body weight in DMH-administered rats. The administration of reserpine substantially diminished oxidative stress, regulated inflammatory cytokine levels, and inhibited the AKT/mTOR axis in DMH-induced rats. Furthermore, reserpine also regulated the activities of xenobiotic-metabolizing enzymes and apoptotic protein levels and reduced the tumor markers in DMH-administered rats. The results of the histopathological analysis also witnessed the anti-cancer roles of reserpine. Conclusion The present work shows that reserpine exhibits significant anti-cancer effects against DMH-induced colon cancer in rats. These findings demonstrate that reserpine has the capacity as an anti-cancer agent to treat colon cancer.