Numerous underexplored plant species are believed to possess considerable potential in combating oxidative stress and its associated health impacts, emphasizing the need for a comprehensive methodological screening approach to assess their antioxidant capacity. This study investigated 375 plant extracts, utilizing both cell-free and cellular methods to evaluate their antioxidant properties. Target-based antioxidant capacity was evaluated by the total phenolic content (TPC) and ferric reducing antioxidant power (FRAP) assays. Cell-based assays employed the H₂DCF-DA probe to measure reactive oxygen species (ROS) levels and the Griess assay to quantify nitric oxide (NO) levels in stressed Caco-2 and RAW264.7 cells, respectively. The highest TPC and FRAP values were found in extracts of Origanum vulgare and Fragaria × ananassa leaves. Several plant extracts significantly reduced stress-induced ROS or NO levels by at least 30%. Distinctive selectivity was noted in certain extracts, favoring the significant reduction of NO (e.g., Helianthus tuberosus extract), of ROS (e.g., Prunus domestica subsp. Syriaca extract), or of both (e.g., Fragaria × ananassa leaf extract). A strong correlation between TPC and FRAP values and moderate correlations between the results of the cell-free and cell-based assays were evident. These findings highlight the great antioxidant potential of underexplored plant extracts and the diversity of the underlying mechanisms, emphasizing the importance of a multifaceted approach for a comprehensive assessment.

Scope: Sea buckthorn (Hippophaes rhamnoides) is capable of ameliorating disturbed glucose metabolism in animal models and human subjects. Here, the effect of sea buckthorn oil as well as of extracts of fruits, leaves, and press cake on postprandial glucose metabolism is systematically investigated.Methods and results: Sea buckthorn did neither exert decisive effects in an in vitro model of intestinal glucose absorption nor did it alter insulin secretion. However, sea buckthorn stimulates GLUT4 translocation to the plasma membrane comparable to insulin, indicative of increased glucose clearance from the circulation. Isorhamnetin is identified in all sea buckthorn samples investigated and is biologically active in triggering GLUT4 cell surface localization. Consistently, sea buckthorn products lower circulating glucose by ≈10% in a chick embryo model. Moreover, sea buckthorn products fully revert hyperglycemia in the nematode Caenorhabditis elegans while they are ineffective in Drosophila melanogaster under euglycemic conditions.Conclusion: These data indicate that edible sea buckthorn products as well as by‐products are promising resources for hypoglycemic nutrient supplements that increase cellular glucose clearance into target tissues.

Intestinal absorption is intrinsically low for lipophilic micronutrients and phytochemicals. Plant extracts acting as bioavailability enhancers can complement for this deficiency by modulation of both, physicochemical and biochemical parameters, in the absorption process. However, these interactions often are limited to specific conditions and the mechanisms and potential synergisms are poorly understood. In this work, we used a human intestinal cell line to characterize the impact of extracts from C. longa (curcuma), Z. officinale (ginger) and P.nigrum (black pepper) on uptake and transport rates of the xanthophylls lutein and zeaxanthin as well as soy isoflavones measured by HPLC-DAD. We found a significant increase in the uptake of lutein in the presence of curcuma extract and enhanced isoflavone transport rates mediated by curcuma and ginger extracts. Combinations of the plant extracts did not lead to any additional increase in uptake or transport rates. By investigation of mixed micelle incorporation efficiency, we could dismiss changes in bioaccessibility as a potential enhancing mechanism in our experimental setup. We further conducted a rhodamine 123 efflux assay and discovered inhibition of P-glycoproteins by the ginger and black pepper extracts, highlighting a plausible route of action leading to increased isoflavone bioavailability.

CD73-derived adenosine plays a major role in damage-induced tissue responses by inhibiting inflammation. Damage-associated stimuli, such as hypoxia and mechanical stress, induce the cellular release of ATP and NAD⁺ and upregulate the expression of the nucleotide-degrading purinergic ectoenzyme cascade, including adenosine-generating CD73. Extracellular NAD⁺ also serves as substrate for mono-ADP-ribosylation of cell surface proteins, which in human cells is mediated by ecto-ADP-ribosyltransferase 1 (ARTC1). Here we explored, whether human CD73 enzymatic activity is regulated by mono-ADP-ribosylation, using recombinant human CD73 in the presence of ARTC1 with etheno-labelled NAD⁺ as substrate. Multi-colour immunoblotting with an anti-etheno-adenosine antibody showed ARTC1-mediated transfer of ADP-ribose together with the etheno label to CD73. HPLC analysis of the enzymatic activity of in vitro-ribosylated CD73 revealed strong inhibition of adenosine generation in comparison to non-ribosylated CD73. Mass spectrometry of in vitro-ribosylated CD73 identified six ribosylation sites. 3D model analysis indicated that three of them (R328, R354, R545) can interfere with CD73 enzymatic activity. Our study identifies human CD73 as target for ARTC1-mediated mono-ADP-ribosylation, which can profoundly modulate its adenosine-generating activity. Thus, in settings with enhanced release of NAD⁺ as substrate for ARTC1, assessment of CD73 protein expression in human tissues may not be predictive of adenosine formation resulting in anti-inflammatory activity.