Octyl ester of ginsenoside compound K as novel anti-hepatoma compound: Synthesis and evaluation on murine H22 cells in vitro and in vivo

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Abstract

Ginsenoside compound K (M1) is the active form of major ginsenosides deglycosylated by intestinal bacteria after oral administration. However, M1 was reported to selectively accumulate in liver and transform to fatty acid esters. Ester of M1 was not excreted by bile as M1 was, which means it was accumulated in the liver longer than M1. This study reported a synthetic method of M1-O, a mono-octyl ester of M1, and evaluated the anticancer property against murine H22 cell both in vitro and in vivo. As a result, both M1 and M1-O showed a dose-dependent manner in cytotoxicity assay in vitro. At lower dose of 12.5 μm, M1-O showed moderate detoxification. Instead, M1-O exhibited significantly higher inhibition in H22-bearing mice than M1. M1-O induced murine H22 tumor cellular apoptosis in caspase-dependent pathway given that pan-caspase inhibitor, Z-VAD-FMK, could reverse the cytotoxicity induced by M1-O. Additionally, pro- and anti-apoptosis proteins, Bcl-2 and Bax, altered and consequently induced increased expression of cleaved caspase-3. Interestingly, cyclophosphamide regimen significantly induced atrophy of spleen and thymus, main immune organs, while M1-O treatment greatly alleviated this atrophy. Collectively, we propose M1-O as a candidate for live cancer treatment.

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