Two new 2-phenoxychromones 1 and 2 and two prenylflavonoids 3 and 4 along with 12 known compounds (5-16) were isolated from the CH2Cl2-soluble fraction of a methanol extract of Epimedium koreanum. Compounds 1, 4, 6, 7, 9, 10, 12, and 15 exhibit inhibitory effects on nitric oxide production with IC50 values ranging from 16.8 to 49.3 μM. Compounds 1, 4, 7, and 12 also showed inhibitory effects on interleukin-1β production with IC50 values ranging from 8.6 to 38.9 μM in RAW 264.7 macrophages.

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Three new neo-clerodane diterpenoids (1-3) along with 12 known compounds (4-15) were isolated from a methanol extract of the aerial parts of Scutellaria barbata. The structures of 1-3 were determined by interpretation of their 1D and 2D NMR spectroscopic data as well as HRESIMS values. All isolated compounds were tested for their inhibitory effects on LPS-induced nitric oxide production in RAW 264.7 macrophages. Compounds 1-4, 7, and 10-12 were found to inhibit nitric oxide production with IC50 values ranging from 20.2 to 35.6 μM.

The Maillard Reaction Products (MRPs) are chemical compounds which have been known to be effective in chemoprevention. Death receptors (DR) play a central role in directing apoptosis in several cancer cells. In our previous study, we demonstrated that (E)-2,4-bis(p-hydroxyphenyl)-2-butenal, a MRP product, inhibited human colon cancer cell growth by inducing apoptosis via nuclear factor-κB (NF-κB) inactivation and G2/M phase cell cycle arrest. In this study, (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate, a new (E)-2,4-bis(p-hydroxyphenyl)-2-butenal derivative, was synthesized to improve their solubility and stability in water and then evaluated against NCI-H460 and A549 human lung cancer cells. (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate reduced the viability in both cell lines in a time and dose-dependent manner. We also found that (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate increased apoptotic cell death through the upregulation of the expression of death receptor (DR)-3 and DR6 in both lung cancer cell lines. In addition to this, the transfection of DR3 siRNA diminished the growth inhibitory and apoptosis inducing effect of (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate on lung cancer cells, however these effects of (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate was not changed by DR6 siRNA. These results indicated that (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate inhibits human lung cancer cell growth via increasing apoptotic cell death by upregulation of the expression of DR3.