美国一项新研究显示，肺癌患者在接受放射治疗期间补充大豆异黄酮可提高放疗功效，而且不会产生副作用。
研究人员把染料木黃酮、黃豆甘原和黄豆黄素3种大豆异黄酮结合起来，用来配合肺癌患者的放射治疗。结果发现，上述3种大豆异黄酮能有效帮助杀灭癌细胞，同时保护正常组织不受辐射伤害。
研究人员解释说，放疗期间，癌细胞会形成一种自我保护机制，而大豆异黄酮却会破坏这种保护机制，削弱癌细胞的脱氧核糖核酸修复能力，从而提高癌细胞对放疗的敏感性；对正常组织来说，大豆异黄酮具有抗氧化作用，因此可以使这些组织免遭放疗伤害。
此前研究曾发现染料木黃酮也具有抗癌功效，但最新研究显示，如果患者同时补充上述３种大豆异黄酮，放疗效果更好。
这项研究成果刊登在国际肺癌研究协会主办的月刊《胸部肿瘤杂志》上。（生物谷Bioon.com）
生物谷推荐原文出处：
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.
