Journal
TOXICOLOGY IN VITRO
Volume 25, Issue 7, Pages 1385-1391Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.tiv.2011.05.009
Keywords
Non-small-cell lung carcinoma; A549; Luteolin; Cytotoxicity; Cell cycle; Apoptosis
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Funding
- National Natural Science Foundation of China [30701098, 30873410, 81073101]
- Natural Science Foundation of Zhejiang Province [Y2090676]
- Jiangsu Province's Outstanding Leader Program of Traditional Chinese Medicine
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In this study, we investigated the underlying molecular mechanism for the potent cell cycle inhibition and pro-apoptotic effect of luteolin (2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4-chromenone) on human non-small-cell lung carcinoma cell line A549. MIT assay showed that luteolin had obvious cytotoxicity on A549 with IC50 of 40.2 mu M at 48 h. Pro-apoptotic effect of luteolin on A549 cells was demonstrated by Hoechst 33258 staining assay and annexin V-FITC/PI double staining analysis. A great quantity of apoptotic cells and increasing G2 phase cells were observed by flow cytometry. Western blotting assay revealed that luteolin activated JNK, increased Bax, promoted procaspase-9 cleavage and activated caspase-3 at last. Assay using TNF alpha, an active agent of NF-kappa B, showed that pretreatment of A549 cells with luteolin could inhibit TNFa induced trans-nuclear of NF-kappa B. In summary, luteolin displayed a significant cytotoxic effect through cell cycle arrest and apoptosis induction in A549 cells. Pro-apoptotic effect was implemented via activating JNK and inhibiting translocation of NF-kappa B (p65). These results suggested that luteolin might have therapeutic potential against NSCLC. (C) 2011 Elsevier Ltd. All rights reserved.
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