Anticarcinogenic effect of brucine on DMBA-induced skin cancer via regulation of PI3K/AKT signaling pathway

Background: Brucine is an alkaloid derived from the natural plant seeds of Strychnos nux-vomica, also known as a medicinal herb, and broadly employed in Chinese medicine for liver cancer. Objectives: The main intention of these hypothesis anticancer effects of brucine on 7,12-dimethylbenz(a)anthracene (DMBA)-induced skin cancer in mouse model through phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) regulating signaling pathway via the suppressive effect on cell proliferation and apoptotic pathways in mouse model. Materials and Methods: Brucine action on DMBA-induced mouse skin body weight, tumor volume, histology, biochemical, molecular marker analysis using spectrophotometric, Western blotting, and real-time polymerase chain reaction analysis. Results: Brucine stifled the lipid peroxidation (TBARS), suggestively augmented the levels of antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione), and brought back the status of xenobiotic enzymes (Cyt-p450, Cyt-b5, and glutathione S-transferases). In brucine administered since skin tissues presented the cell proliferative protein marker expression of PI3K, and AKT were downregulated compared to the DMBA-applied skin tumor tissues protein. Further, brucine has downregulated the proliferating cell nuclear antigen, cyclin-D1, and p53 expressions. In the apoptotic expression, markers such as Bcl-2, Bax, caspase-3, and caspase-9 were upregulated compared to the DMBA-induced skin cancer. From these data, we diseased and brucine potential to suppress the proliferative cell markers induces apoptotic expressions. Conclusion: The current search settled that administering brucine chemopreventive and chemotherapeutic effect means for the cancer management in clinical tactic.

Automated summary

The study found that brucine has anticancer effects on DMBA-induced skin cancer in a mouse model by suppressing cell proliferation and inducing apoptosis through regulating the PI3K/AKT signaling pathway.