Cucurbitacin and volatile compound profiling reveals independent domestication of cucumber (Cucumis sativus L.) fruit.

Profiling of metabolites that confer bitter taste and flavor to cucumber products is necessary to produce preferred products. In this study, cucurbitacins A, B, C, D, E, and I and untargeted volatile compounds were analyzed using the fruit of 69 inbred cucumber of diverse cultivars. Only cucurbitacin C was detected in six inbreds. They were classified into four clusters based on the profiles of cucurbitacins and volatile compounds. Clusters 2 and 3 showed the largest difference with the highest and lowest volatile contents, respectively. Clusters 1 and 4 showed different fruit phenotypes of length and color. Fifteen F1 hybrids from selected inbreds were analyzed. Total volatile compound (TVC) content, especially for the alcohol content, was lower in the F1 hybrids than the mid-parent values, and the ratio of aldehyde to TVC was increased. This profiling will contribute to produce cucumber products with no bitter taste and improved flavor.

Suppression of inducible nitric oxide synthase expression by nyasol and broussonin A, two phenolic compounds from Anemarrhena asphodeloides, through NF-κB transcriptional regulation in vitro and in vivo.

Anemarrhena asphodeloides is widely used in traditional Chinese medicine, and is known to possess antidiabetic and anti-inflammatory properties. Because inducible nitric oxide synthase (iNOS) plays an important role in inflammation, we investigated the inhibitory effects of two known phenolic compounds, nyasol (1) and broussonin A (2), from A. asphodeloides, on iNOS and its plausible mechanism of action. Compounds 1 and 2 exhibited inhibitory effects on nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Compounds 1 and 2 also suppressed the expressions of iNOS protein and mRNA. Moreover, compounds 1 and 2 suppressed the expression of inflammatory cytokines such as interleukin-1ß (IL-1ß) and interferon-ß (IFN-ß). They also inhibited the transcriptional activity of NF-κB and degradation of IκB-α, as well as the activation of Akt and ERK in LPS-stimulated RAW 264.7 cells. In in vivo animal model, compounds 1 and 2 significantly inhibited TPA-induced mouse ear edema. These results suggest that 1 and 2 suppress LPS-stimulated iNOS expression at the transcriptional level through modulating NF-κB and down-regulation of the Akt and ERK signaling pathways. Taken together, these findings indicate that the suppressive effects of 1 and 2 on iNOS expression might provide one possible mechanism for their anti-inflammatory activities.