The inhibition of tumor-cell proliferationbyan organicsolvent extract from the solid-state fermentation of Phellinus baumii mycelia inoculated in rice medium was investigated in vitro. The active compounds inhibiting tumor-cell proliferation were characterized. Results revealed that all (petroleum ether, chloroform, ethyl acetate, and butanol) fractions inhibited tumor-cell proliferation in a dose-dependent fashion. The ethyl acetate extract had the highest inhibitory effecton tumor-cell proliferation, and the butanol fraction had the lowest. Six compounds were isolated and purified from the ethyl acetate extract of P. baumii mycelia by the tandem application of silica-gel column chromatography (SGCC), high-speed countercurrent chromatography (HSCCC), and preparative HPLC. These compounds were identified by NMR and electrospray ionization-mass spectrometry (ESI-MS) spectroscopic methods as ergosterol (RF1), ergosta-7,22-dien-3β-yl pentadecanoate (RF3), 3,4-dihydroxy benzaldehyde(RF6), inoscavinA (RF7), baicalein(RF10), and 24-ethylcholesta-5,22-dien-3β-ol (RF13). To further clarify the activity of these compounds, the cell-proliferation-inhibition tests of these compounds on various tumor cells were carried out and evaluatedin vitro. Results suggested that compounds RF6, RF7, and RF10 had potent inhibition effects on the proliferation of a series of tumor cell lines, including K562, L1210, SW620, HepG2, LNCaP, and MCF-7cells. These findings indicated that P. baumii mycelia produced by solid-state fermentation in rice canbe used to obtain active compounds with the ability to inhibittumor-cell proliferation.

Phellinus baumii was used for fermentation, and 3 corresponding ethanol extracts were obtained by 3 different methods: extract I, liquid fermentation; extract II, solid fermentation in polypropylene plastic bags with medium mainly consisting of sawdust and wheat bran; and extract III, solid fermentation in culture bottles with medium mainly consisting of rice. Ethanol extract I presented the best inhibition ability on HepG2 cell growth; inhibiting rates were 48.2% and 65.0% at doses of 10 and 100 µg/mL, respectively. Ethanol extracts II and III had a better regeneration effect on injured PC12 neural cells than extract I. The superoxide radical, hydrogen peroxide radical, and DPPH radical scavenging activities of ethanol extract III was better than those of the other 2 extracts.