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Year : 2019  |  Volume : 15  |  Issue : 64  |  Page : 288-297

Caesalpinia pulcherrima arrests cell cycle and triggers reactive oxygen species-induced mitochondrial-mediated apoptosis and necroptosis via modulating estrogen and estrogen receptors

1 Department of Pharmacology, Dr. Rafiq Zakaria Campus, Y. B. Chavan College of Pharmacy, Aurangabad, Maharashtra, India
2 Department of Medicinal Chemistry, R. C. Patel Institute of Pharmaceutical Education and Research, Shirpur, Maharashtra, India

Correspondence Address:
Santosh Namdeo Mokale
Dr. Rafiq Zakaria Campus, Y. B. Chavan College of Pharmacy, Aurangabad - 431 001, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_100_19

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Background: Caesalpinia pulcherrima belonging to the family Fabaceae is used in India as a traditional medicine for a variety of ailments. Globally, traditional medicines are presently being used for the treatment of cancer. Objective: The present study was aimed at investigating the chemomodulatory potential of C. pulcherrima flowers in breast cancer and explaining its possible mechanism. Materials and Methods: The cytotoxic potential of ethyl acetate fraction of C. pulcherrima (EAFCP) flower was tested in MCF-12A (normal breast), MCF-7 (estrogen receptor [ER] positive), and MDA-MB-453 (human epidermal growth factor receptor 2 positive) human breast cancer cells by sulforhodamine B assay. Chemomodulatory potential was evaluated in vivo against N-methyl-N-nitrosourea (MNU)-induced mammary carcinoma in female Sprague Dawley® rats. The mechanism for anticancer potential was screened by in vitro studies involving Annexin V-FITC assay (apoptosis), cell cycle patterns, intracellular reactive oxygen species, and mitochondrial membrane potential measurement (FACS based) followed by docking study on estrogen receptor-alpha (ER-α). Results: The fractions showed perceptible cell growth inhibition potency (IC50<50 μg/ml) in MCF-7 breast cancer cells. In MNU-treated animals, antioxidant enzymes and histological examination showed statistically significant (P < 0.001) changes. Treatment of MCF-7 cells with EAFCP reduced cell growth rate by a mechanism associated with both apoptotic and necrotic cell death. Molecular docking study further showed that rutin and catechin have a comparable binding affinity for the ER-α. Conclusion: In this study, we confirmed that EAFCP was most effective in reducing cell viability, scavenging physiological oxidant species, and causing mitochondria-mediated apoptosis and necroptosis in MCF-7 cell by selectively modulating the functions of ER-α.

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