Polygonum cuspidatum is a widely grown crop with a rich source of polydatin (also called piceid) for resveratrol production. Resveratrol is produced from piceid via enzymatic cleavage of the sugar moiety of piceid. In this study, Dekkera bruxellensis mutants were selected based on their high p-nitrophenyl-β-d-glucopyranoside and piceid conversion activities. The enzyme responsible for piceid conversion was a heterodimeric protein complex that was predominantly secreted to the extracellular medium and consisted of two subunits at an equal ratio with molecular masses of 30.5 kDa and 48.3 kDa. The two subunits were identified as SCW4p and glucan-β-glucosidase precursor in D. bruxellensis. Both proteins were individually expressed in Saccharomyces cerevisiae exg1Δ mutants, which lack extracellular β-glucosidase activity, to confirm each protein's enzymatic activities. Only the glucan-β-glucosidase precursor was shown to be a secretory protein with piceid deglycosylation activity. Our pilot experiments of piceid bioconversion demonstrate the possible industrial applications for this glucan-β-glucosidase precursor in the future.

Background: Polygonum cuspidatum (Hu Zhang) is a polyphenol-rich botanical in which resveratrol occurs at low levels mainly as polydatin. In this study, we generated a microbially converted P. cuspidatum extract (CPE) with markedly enriched resveratrol content from the unconverted P. cuspidatum extract (PE), and evaluated its anticancer efficacy and safety in comparison with those of the unconverted extract. Methods: High-performance liquid chromatography (HPLC), A549 cell-based assays, an A549 xenograft model, and a 28-day repeated-dose rat study were performed. Results: HPLC showed near-complete depletion of polydatin, marked enrichment of resveratrol, and a modest reduction in emodin. CPE more effectively inhibited A549 cell proliferation and migration than PE, suppressed NLRP3 inflammasome and nuclear factor kappa B (NFκB) signaling, and promoted reactive oxygen species (ROS) accumulation and mitochondrial apoptosis. Oral CPE also significantly reduced tumor growth in an A549 xenograft model. In a 28-day repeated-dose rat study, no treatment-related abnormalities were observed in blood biochemistry or histopathology. Conclusions: These findings support CPE as a promising functional food ingredient.