1. Insights into Osteogenesis Induced by Crude Brassicaceae Seeds Extracts: A Role for Glucosinolates.
- Author
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Gambari, Laura, Pagnotta, Eleonora, Ugolini, Luisa, Righetti, Laura, Amore, Emanuela, Grigolo, Brunella, Filardo, Giuseppe, and Grassi, Francesco
- Abstract
Background/Objectives: Crude extracts from the Brassica genus have recently emerged as promising phytochemicals for preventing bone loss. While the most documented evidence suggests that their general biological activity is due to glucosinolates' (GLSs') hydrolysis products, the direct activity of GLSs is beginning to be uncovered. However, the contribution of GLSs to the bone-sparing activity of crude Brassicaceae extracts has seldom been addressed. Here, we aimed to gain insights into this gap by studying in the same in vitro model of human osteogenesis the effect of two Brassica seed extracts (Eruca sativa and Lepidium sativum) obtained from defatted seed meals, comparing them to the isolated GLSs most represented in their composition, glucoerucin (GER) and glucotropaeolin (GTL), for Eruca sativa and Lepidium sativum, respectively. Methods: Osteogenic differentiation of human mesenchymal stromal cells (hMSCs) was assessed by alizarin red staining assay and real-time PCR, respectively, evaluating mineral apposition and mRNA expression of specific osteogenic genes. Results: Both Brassica extracts and GLSs increased the osteogenic differentiation, indicating that the stimulating effect of Brassica extracts can be at least partially attributed to GLSs. Moreover, these data extend previous evidence of the effect of unhydrolyzed glucoraphanin (GRA) on osteogenesis to other types of GLSs: GER and GTL. Notably, E. sativa extract and GTL induced higher osteogenic stimulation than Lepidium sativum extract and GER, respectively. Conclusions: Overall, this study expands the knowledge on the possible application of Brassica-derived bioactive molecules as natural alternatives for the prevention and treatment of bone-loss pathologies. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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