α-Mangostin Shows Chemopreventive Activity in Benzo[a]pyrene-induced Lung Cancer in Mice Via Regulation of Apoptosis and Tumor Biomarkers

ABSTRACT

Background: Lung cancer is a serious disease affecting millions of individuals globally, defined by the unregulated proliferation of abnormal cells in the lungs. It is the primary cause of cancer-associated fatalities worldwide, representing a significant portion of cancer incidence and mortality rates. Objectives: This work was dedicated to assessing the anti-cancer activity of α-mangostin against benzo[a]pyrene (B[a]P)-induced lung cancer in mice model. Materials and Methods: Lung tumorigenesis was initiated in Swiss mice with oral treatment of B[a]P for 4 consecutive weeks. Mice were treated with α-mangostin following B[a]P induction in mice for 16 weeks. The body and lung weights and tumor incidences were assessed in the experimental mice after the conclusion of the treatments. The concentrations of oxidant and antioxidant markers, tumor biomarkers, mitochondrial enzymes, and apoptotic protein markers in the experimental mice were assessed using the commercial diagnostic kits. The immunohistochemical analysis was performed on the lung tissues to assess the expression of the proliferating cell nuclear antigen (PCNA) protein. Results: Both pre- and post-treatments of α-mangostin (25 mg/kg) significantly enhanced body weight while reducing lung weight and tumor incidences in the B[a]P-induced mice. The α-mangostin treatment effectively increased the antioxidants and vitamins and diminished the tumor biomarker concentrations in the mice with lung cancer. Furthermore, the α-mangostin treatment considerably increased the mitochondrial enzyme concentrations and regulated the apoptotic proteins in the lung tissues of B[a]P-induced mice. In addition, the PCNA protein expression was reduced by the α-mangostin treatment in the lung tissues. Conclusion: In conclusion, our findings demonstrate that α-mangostin exhibits chemopreventive properties in lung cancer initiated by B[a]P in mice, suggesting its potential to enhance chemotherapy approaches for lung cancer.

KEYWORDS

• Neuron-specific enolase
• apoptosis
• cytochrome c
• α-mangostin
• lung cancer

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• DOI10.1177/09731296251341499Copy

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