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Baohuoside I, a flavonoid isolated from Epimedium koreanum Nakai, acts as an inhibitor of CXCR4, downregulates CXCR4 expression, induces apoptosis and shows anti-tumor activity.
Baohuoside I is an inhibitor of CXCR4, and downregulates CXCR4 expression at 12-25 μM. Baohuoside I (0-25 μM) suppresses NF-κB activation in a dose-dependent manner, suppresses CXCL12 induced the invasion of cervical cancer cells. Baohuoside I also inhibits invasion of breast cancer cells[1]. Baohuoside I inhibits A549 cell viability, with IC50s of 25.1 μM at 24 h, 11.5 μM and 9.6 μM at 48 h and 72 h, respectively. Baohuoside I ((25 μM) suppresses the caspase cascade in A549 cells, elevates ROS levels and activates JNK and p38MAPK signaling cascade[2]. Baohuoside I (3.125, 6.25, 12.5, 25.0 and 50.0 μg/mL) significantly and dose-dependently blocks the growth of esophageal squamous cell carcinoma Eca109 cells, with an IC50 of 4.8 μg/mL at 48 h[3].
Baohuoside I (25 mg/kg) decreases β-catenin protein levels, cyclin D1 and survivin expression in nude mice[3].
References:
[1]. Kim B, et al. Baohuoside I suppresses invasion of cervical and breast cancer cells through the downregulation of CXCR4 chemokine receptor expression. Biochemistry. 2014 Dec 9;53(48):7562-9.
[2]. Song J, et al. Reactive oxygen species-mediated mitochondrial pathway is involved in Baohuoside I-induced apoptosis in human non-small cell lung cancer. Chem Biol Interact. 2012 Jul 30;199(1):9-17.
[3]. Wang L, et al. The flavonoid Baohuoside-I inhibits cell growth and downregulates survivin and cyclin D1 expression in esophageal carcinoma via β-catenin-dependent signaling. Oncol Rep. 2011 Nov;26(5):1149-56.
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