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天然和合成异黄酮在慢性病防治中的应用

Natural and synthetic isoflavones in the prevention and treatment of chronic diseases.

作者信息

Brandi M L

机构信息

Department of Clinical Physiopathology, University of Florence, Italy.

出版信息

Calcif Tissue Int. 1997;61 Suppl 1:S5-8. doi: 10.1007/s002239900376.

DOI:10.1007/s002239900376
PMID:9263608
Abstract

The evidence that natural isoflavones protect against several chronic diseases is both observational and experimental. In humans, epidemiologic findings clearly show a higher incidence of some common types of cancer (i.e., breast, prostate, and colon) and of coronary heart diseases in Western populations exposed to limited amounts of soybean isoflavones (i.e., genistein, daidzein) in the diet. Further evidence for cancer and cardiac protection and antiatherogenic effects resulting from soybean isoflavones administration has been noted in various experimental animal models. Isoflavones may also prevent postmenopausal bone loss and osteoporosis. In fact, genistein has been reported to be as active as estrogens in maintaining bone mass in ovariectomized rats. Moreover, the synthetic isoflavone derivative ipriflavone is able to reduce bone loss in various types of animal models of experimental osteoporosis providing a rationale on its use in the prevention and treatment of postmenopausal and senile osteoporosis in humans. The mechanism through which isoflavones may exert the above-mentioned effects seems to depend, at least in part, on their mixed estrogen agonist-antagonist properties. An alternative hypothetical mechanism could derive from other biochemical actions of isoflavones such as inhibition of enzymatic activity, in particular protein kinases, or activation of an "orphan" receptor distinct from the estrogen type I receptor.

摘要

天然异黄酮预防多种慢性疾病的证据既有观察性的,也有实验性的。在人类中,流行病学研究结果清楚地表明,西方人群饮食中大豆异黄酮(如染料木黄酮、大豆苷元)摄入量有限,某些常见类型癌症(即乳腺癌、前列腺癌和结肠癌)以及冠心病的发病率较高。在各种实验动物模型中也发现了大豆异黄酮给药对癌症、心脏保护和抗动脉粥样硬化作用的进一步证据。异黄酮还可能预防绝经后骨质流失和骨质疏松症。事实上,据报道,染料木黄酮在维持去卵巢大鼠骨量方面与雌激素一样有效。此外,合成异黄酮衍生物依普黄酮能够减少各种实验性骨质疏松动物模型中的骨质流失,这为其用于预防和治疗人类绝经后和老年性骨质疏松症提供了理论依据。异黄酮发挥上述作用的机制似乎至少部分取决于其混合的雌激素激动剂 - 拮抗剂特性。另一种假设机制可能源于异黄酮的其他生化作用,如抑制酶活性,特别是蛋白激酶,或激活不同于雌激素I型受体的“孤儿”受体。

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