Background:
Liquiritin, a flavonoid isolated from Glycyrrhiza, is a potent and competitive AKR1C1 inhibitor with IC50s of 0.62 μM, 0.61 μM, and 3.72μM for AKR1C1, AKR1C2 and AKR1C3, respectively. Liquiritin efficiently inhibits progesterone metabolism mediated by AKR1C1 in vivo[1]. Liquiritin acts as an antioxidant and has neuroprotective, anti-cancer and anti-inflammatory activity[2].
Liquiritin can target the residues Ala-27, Val-29, Ala-25, and Asn-56 of AKR1C1[1]. Liquiritin (50 μM; 6 hours) results in 85.00% of reduction in progesterone metabolism, which is mediated by Aldo-keto reductase family 1 member C1 (AKR1C1) enzymatic activity in HEC-1-B cells[1]. Liquiritin (100 μM) increases glucose-6-phosphate dehydrogenase expression on B65 neuroblastoma cells[2].
参考文献:
[1]. Zeng C, et al. Liquiritin, as a Natural Inhibitor of AKR1C1, Could Interfere With the Progesterone Metabolism. Front Physiol. 2019 Jul 3;10:833.
[2]. Nakatani Y, et al. Neuroprotective effect of liquiritin as an antioxidant via an increase in glucose-6-phosphate dehydrogenase expression on B65 neuroblastoma cells. Eur J Pharmacol. 2017 Nov 15;815:381-390.
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