Braquet P, Senn N, Robin J P, Esanu A, Godfraind T, Garay R
Pharmacol Res Commun. 1986 Mar;18(3):227-39. doi: 10.1016/0031-6989(86)90121-9.
Several mammalian lignans, particularly enterolactone, 3-oxy-methyl enterolactone and prestegane B are able to inhibit Na+, K+-pump activity in human red cells with IC50 of about 1 mM. The inhibition of Na+, K+-pump activity by mammalian lignans have the following properties: the IC50 for ouabain remains unchanged suggesting a noncompetitive inhibition. The apparent affinity for internal Na+ and maximal rate of cation translocation are both diminished. The above inhibition of the Na+, K+-pump was obtained at doses 2-3 orders of magnitude higher than those required for ouabain. However we cannot exclude that a glycosyl- (and/or butenolide)-derivative of enterolactone could be one endogenous ouabain-like factor.
几种哺乳动物木脂素，特别是肠内酯、3-氧甲基肠内酯和前木脂素B能够抑制人红细胞中的Na +，K + -ATP酶活性，IC50约为1 mM。哺乳动物木脂素对Na +，K + -ATP酶活性的抑制具有以下特性：哇巴因的IC50保持不变，表明是非竞争性抑制。对内部Na +的表观亲和力和阳离子转运的最大速率均降低。上述对Na +，K + -ATP酶的抑制是在比哇巴因所需剂量高2-3个数量级的剂量下获得的。然而，我们不能排除肠内酯的糖基-（和/或丁烯内酯）衍生物可能是一种内源性哇巴因样因子。
