Licochalcone A

UGT1A1:0.97 μM

在感染了L. major的小鼠中，licochalcone A (5 mg/kg, i.p.) 完全防止了病损的发展。在感染了L. donovani的小鼠中，licochalcone A (150 mg/kg, p.o.) 使肝脏和脾脏的寄生虫负荷分别减少了65%以上和85%。[2] 在接种了CT-26细胞的Balb/c小鼠中，licochalcone A (1 mg/kg, p.o.) 抑制了肿瘤的生长，同时减轻了顺铂引起的肾毒性和肝毒性。[4]

Licochalcone A 显著抑制了在人类的MDMs和U937细胞中L. major无鞭毛体的体外生长。[1] Licochalcone A 对所有经测试的革兰氏阳性细菌表现出抗菌效果，尤其是对所有经测试的Bacillus spp.，MICs在2到3 micrograms/mL之间。[3] 在CT-26结肠癌细胞中，Licochalcone A 降低了细胞活力和DNA合成。[4] Licochalcone A 还干扰MAPK信号通路，引发ROS生成，诱导氧化应激，并因此引起BGC细胞凋亡。[5]

DMSO:55 mg/mL (162.53 mM);Ethanol:67 mg/mL (197.99 mM);H2O:< 1 mg/mL (insoluble or slightly soluble);15% Cremophor EL:5 mg/mL (14.78 mM);Chloroform:Soluble

The viability of CT-26 mouse colon cancer cells is determined via a MTT assay. In brief, colon cancer cells are seeded onto each well of a 96-well plate with DMEM containing 10% FBS and cultured to adhere overnight. The cells are then treated with various concentrations of LCA in serum-free medium for 24 and 72 hr, respectively. Twenty microlitres of a MTT solution (5 mg/ml) is added to each well, and the cells are incubated for 4 hr at 37°. The medium is then removed, and 200 μL of dimethyl sulfoxide is added to each well. The absorbance is determined at 570 nm using a microplate reader.(Only for Reference)