Moringa oleifera Lam. is rich in phytochemical compounds especially glucosinolates (GSs) and isothiocyanates (ITCs), which are active compounds for cancer chemoprevention benefits of Brassicaceae vegetables. In this study, we determined the total contents of GSs and ITCs and their specific profiles in different Moringa tissues including seeds, stems, leaves and roots. Seeds (seeds with shell and seed kernel) showed significantly higher levels of total GSs and ITCs than that of other Moringa tissues. The hydrogen sulfide (H2S) releasing capacity of total ITCs extracted from different Moringa tissues was determined by lead (II) acetate assay in 24-well plates. The H2S releasing capacity of different Moringa tissues were evaluated and compared. Moringa seeds showed the highest H2S releasing capacity, followed by roots, leaves and stems. Our results suggest that Moringa based foods may exhibit health benefits due to its GSs and ITCs contents that are the precursors for H2S, in addition to the recognized action mechanisms of ITCs.
Osteoarthritis (OA) is the leading degenerative joint disease and featured by articular cartilage destruction, where chondrocyte apoptosis plays a critical role. Semaphorin-3A (Sema3A) has been implicated in OA chondrocyte physiology. In this study we aimed to uncover how Sema3A signaling is regulated in chondrocytes and investigate its role in OA chondrocyte survival. Here, we report that Sema3A and its receptor neuropilin-1 (Nrp1) are synchronously upregulated in cartilage chondrocytes of knee OA patients. Their expressions in chondrocytes could be induced by the stimulation of proinflammatory cytokines IL-1β and TNF-α and subsequent transcriptional activation orchestrated by C/EBPβ. The resulting excessive Sema3A signaling promotes chondrocyte apoptosis through impairing PI3K/Akt prosurvival signaling. These findings indicate a regulatory mechanism and a proapoptotic function of aberrant Sema3A signaling in OA chondrocytes, and suggest that targeting Sema3A signaling might interfere OA pathogenesis.
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