Abstract
Objective: The present study was designed to investigate the anti-melanoma activity of the ethyl acetate fraction of Lawsonia alba lam leaves (ELA) against B16F10 cells.Methods: Cytotoxicity of ELA on B16F10 cells was determined by MTT assay and supported with the morphology of apoptotic and necrotic cells under phase-contrast microscope, fluorescence microscopy with AO/EtBr, confocal microscopy with PI, Agarose gel electrophoresis and Annexin V-FITC/PI staining, mitochondrial membrane potential and cell cycle arrest by FACS was also performed on B16F10 cells.Results: Cytotoxic effect of ELA on B16F10 melanoma cell was confirmed by MTT assay with an IC50 value of 14.10μg/ml. Morphological study showed arrays of both the nuclear changes including chromatin condensation and apoptotic body formation indicating that the treatment with ELA and 5-Fluorouracil (standard) causes apoptotic changes in the melanoma cells compared to the untreated control. Agarose gel electrophoresis study showed fragmented DNA in the form of ladder. The depolarization of mitochondrial membrane potential was confirmed. Flow cytometric analysis showed appreciable number of cells in early apoptotic stage. The cells were arrested mostly in G0/G1 phase of cell cycle.Conclusion: Ethyl acetate fraction of Lawsonia alba L. leaves possesses potent apoptotic activity against B16F10 cells.
Highlights
Cancer is the cell proliferation independent of growth factor regulation with apoptosis resistance and angiogenesis, leading to the disruption of homeostatic condition therapy to tumorigenesis
Acridine orange and ethidium bromide stained B16F10 melanoma cells revealed nuclear chromatin condensation and apoptotic body formation thereby indicating the occurrence of apoptosis
Our results clearly indicated that Ethyl acetate fraction of Lawsonia alba leaves (ELA) exert cytotoxicity on B16F10 melanoma cells through apoptosis
Summary
Cancer is the cell proliferation independent of growth factor regulation with apoptosis resistance and angiogenesis, leading to the disruption of homeostatic condition therapy to tumorigenesis. Melanoma is an aggressive and refractory cancer derived from melanocytes [1]. The incidence of melanoma has been continuously increasing worldwide and becoming a huge public health issue [2]. The standard means of treating melanoma include surgery, radiation therapy, and chemotherapy [3]. (The treatment of melanoma disease largely depends upon early diagnosis [4]. Drug resistance in melanoma mainly occurred through dysregulation of apoptosis, whereas drug transport, detoxification, and enhanced DNA repair may exert a function [5]. Induction of apoptosis deliberated the major target of anticancer chemotherapeutic strategies for melanoma [6]
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