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Wolfberry water soluble extracts selectively induce leukemia cell apoptosis
Author(s) -
Ji Hua,
Lin Dingbo
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.639.22
Subject(s) - jurkat cells , apoptosis , cell growth , cyclin b1 , cell cycle , microbiology and biotechnology , chemistry , leukemia , cyclin dependent kinase 1 , biochemistry , biology , t cell , immunology , immune system
Objective Our aim was to determine whether wolfberry water soluble extracts (WWSE) selectively induce apoptosis of leukemia cells, but not normal T‐cells in culture. Methods Contents of taurine, betaine, and rutin of wolfberry water soluble extracts were measured by TLC and/or HPLC. Leukemia Jurkat cells and normal human T cells were treated with WWSE for 48 hours. Cell proliferation, apoptosis, and alteration of gene expression and protein phosphorylation were determined by BrdU assay, flow cytometry, Western blot, and/or immuneprecipitation. Results WWSE were enriched in carbohydrates (73.4 ± 4.5 % (w/w)), polyphenolics (1555 ± 112 mg quercetin equivalent/100 g freeze dry powder) including 213 mg rutin/100 g freeze dry powder, betaine (374 ± 25 mg/100 g freeze dry powder), and had enhanced antioxidant activity (7771 ±207 μmol Trolox equivalent/100 g freeze dry powder). WWSE had no effect on growth and proliferation of normal human T cells, but inhibited Jurkat cell proliferation, induced cycle arrest at the G2/M phase in a dose dependent manner starting at 1 mg/mL for 48 h. Furthermore, WWSE down‐regulated SIRT1 protein expression, inactivated cyclin‐dependent kinase 1 (CDK1), and disrupted the interaction of SIRT1 with CDK1 in Jurkat cells only. Knockdown of SIRT1 by specific siRNA caused inactivation of CDK1 leading to Jurkat cell apoptosis. Conclusions Data suggested that consumption of wolfberry could be an efficacious dietary strategy for preventing leukemia. Grant Funding Source: National Institutes of Health COBRE Grant P20‐RR‐017686 and the Kansas State University Cancer Center Research Initiative Award