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Tropical Journal of Pharmaceutical Research
Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria
ISSN: 1596-5996
EISSN: 1596-9827
Vol. 15, No. 1, 2016, pp. 39-45
Bioline Code: pr16006
Full paper language: English
Document type: Research Article
Document available free of charge

Tropical Journal of Pharmaceutical Research, Vol. 15, No. 1, 2016, pp. 39-45

 en Luteoloside Inhibits Proliferation of Human Chronic Myeloid Leukemia K562 Cells by Inducing G2/M Phase Cell Cycle Arrest and Apoptosis
Shao, Jun-Li; Liang, Hai-Rong & Dai, Juan-Xiu


Purpose: To investigate the effects of luteoloside on the proliferation of human chronic myeloid leukemia K562 cells and whether luteoloside induces cell cycle arrest and apoptosis in K562 cells.
Methods: Luteoloside’s cytotoxicity was assessed using a cell counting kit. Cell cycle distribution was analysed by flow cytometry after propidium iodide (PI) staining. Cell apoptosis was assayed with apoptosis detection kit and Hoechst staining followed by observation under a fluorescence microscope. The expression of cell cycle- and apoptosis-related proteins was examined by Western blot analysis.
Results: Luteoloside inhibited the proliferation of K562 cells in a dose- and time- dependent manner (IC50 = 30.7 μM) with less toxicity in a normal human cell line (IC50 = 91.8 μM). Moreover, antiproliferative effect of luteoloside was accompanied with G2/M phase arrest(p < 0.05 or p<0.01) and apoptosis(p < 0.01 or p < 0.001). Further studies revealed that the expression level of cyclinB1 was down-regulated by luteoloside treatment. Furthermore, luteoloside treatment also increased proapoptotic protein Bax expression and decreased anti-apoptotic protein Bcl-2 expression.
Conclusion: These results suggest that the inhibitory effect of luteoloside on K562 cell proliferation is associated with inducing G2/M phase arrest and apoptosis, and that luteoloside is worth further studying for anticancer potential.

Luteoloside; Myeloid leukemia; Proliferation; Cell cycle arrest; Apoptosis; Anticancer

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