美國一項(xiàng)新研究顯示，肺癌患者在接受放射治療期間補(bǔ)充大豆異黃酮可提高放療功效,，而且不會產(chǎn)生副作用,。
研究人員把染料木黃酮、黃豆甘原和黃豆黃素3種大豆異黃酮結(jié)合起來,，用來配合肺癌患者的放射治療,。結(jié)果發(fā)現(xiàn)，上述3種大豆異黃酮能有效幫助殺滅癌細(xì)胞，同時保護(hù)正常組織不受輻射傷害,。
研究人員解釋說,，放療期間，癌細(xì)胞會形成一種自我保護(hù)機(jī)制,，而大豆異黃酮卻會破壞這種保護(hù)機(jī)制,，削弱癌細(xì)胞的脫氧核糖核酸修復(fù)能力，從而提高癌細(xì)胞對放療的敏感性,；對正常組織來說,，大豆異黃酮具有抗氧化作用，因此可以使這些組織免遭放療傷害,。
此前研究曾發(fā)現(xiàn)染料木黃酮也具有抗癌功效,，但最新研究顯示，如果患者同時補(bǔ)充上述３種大豆異黃酮,，放療效果更好,。
這項(xiàng)研究成果刊登在國際肺癌研究協(xié)會主辦的月刊《胸部腫瘤雜志》上。（生物谷Bioon.com）
生物谷推薦原文出處：
Journal of Thoracic Oncology, 2011; : 1 DOI: 10.1097/JTO.0b013e31821034ae
Soy Isoflavones Augment Radiation Effect by Inhibiting APE1/Ref-1 DNA Repair Activity in Non-small Cell Lung Cancer
Singh-Gupta, Vinita PhD*; Joiner, Michael C. PhD*; Runyan, Lindsay BSc*; Yunker, Christopher K. BSc*; Sarkar, Fazlul H. PhD?; Miller, Steven MD*; Gadgeel, Shirish M. MD?; Konski, Andre A. MD*; Hillman, Gilda G. PhD*
Introduction: Soy isoflavones sensitize cancer cells to radiation both in vitro and in vivo. To improve the effect of radiotherapy for non-small cell lung cancer, we assessed the potential of using a complementary approach with soy isoflavones.
Methods: Human A549 non-small cell lung cancer cells were treated with soy isoflavones, radiation, or both and tested for cell growth. DNA double-strand breaks (DSBs) were detected by immunostaining for γ-H2AX foci. Expressions of γ-H2AX, HIF-1α, and APE1/Ref-1 were assessed by Western blots. DNA-binding activities of HIF-1α and NF-κB transcription factors were analyzed by electrophoretic mobility shift assay.
Results: Soy isoflavones increased A549 cell killing induced by radiation. Multiple γ-H2AX foci were detectable at 1 hour after radiation but decreased at 24 hours after radiation. Soy isoflavones also caused DNA DSBs, but γ-H2AX foci increased over time. Soy isoflavones and radiation caused an increase in γ-H2AX foci, which persisted at 24 hours, indicating both increased DNA damage and inhibition of repair. Soy isoflavones inhibited the radiation-induced activity of the DNA repair/redox enzyme APE1/Ref-1 and the transcription factors NF-κB and HIF-1α. E3330, which inhibits the redox activity of APE1/Ref-1, did not alter the repair of radiation-induced DSBs. Methoxyamine, which inhibits APE1/Ref-1 DNA repair activity, partly blocked the decrease in radiation-induced DSBs at 24 hours, suggesting partial mitigation of radiation-induced DNA repair akin to the effect of soy combined with radiation, in agreement with cytotoxic assays.
Conclusions: Inhibition of APE1/Ref-1 DNA repair activity by soy could be involved in the mechanism by which soy alters DNA repair and leads to cell killing.
