400882-07-7 Purity
95%
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Specification
ε-Viniferin has demonstrated significant potential in regulating neutrophil activity. This study explores its role in inhibiting the respiratory burst induced by N-formyl-L-methionyl-L-leucyl-l-phenylalanine (fMLP) in human neutrophils. ε-Viniferin effectively suppressed fMLP-induced superoxide anion production in a concentration-dependent manner (IC50 = 2.30 ± 0.96 μM for formyl peptide receptor 1 (FPR1) and 9.80 ± 0.21 μM for FPR1,2), without influencing superoxide production induced by formyl peptide receptor 2 (FPR2) agonist WKYMVM. Mechanistically, ε-viniferin inhibited fMLP-induced activation of ERK, Akt, Src, and intracellular calcium mobilization, specifically targeting FPR1. The compound also prevented the binding of FITC-fMLP to FPR1, further confirming its role as a non-competitive, reversible antagonist of FPR1. Additionally, synergistic inhibition of superoxide production was observed when ε-viniferin was combined with an FPR2 antagonist (WRW4), but not with an FPR1 antagonist (cyclosporine H). These findings highlight ε-viniferin's potential as a therapeutic agent in inflammatory conditions driven by excessive neutrophil activation.
This study evaluates the antiproliferative and apoptotic effects of ε-viniferin in non-small cell lung cancer (A549), melanoma (A2058), and osteosarcoma (HOS and U2OS) cell lines. ε-Viniferin demonstrated significant growth inhibition in A549, HOS, and U2OS cells. Notably, ε-viniferin showed superior antiproliferative effects on HOS cells compared to α-viniferin, with the latter having a stronger effect on A549 cells. The combination of both compounds yielded a synergistic effect in A549 cells, enhancing the antiproliferative response compared to either compound alone.
Mechanistically, ε-viniferin and α-viniferin induced apoptosis via distinct molecular pathways. α-Viniferin triggered apoptosis in HOS cells by modulating the c-Jun N-terminal kinase (JNK) pathway and promoting cleavage of Poly (ADP-ribose) polymerase (PARP). In contrast, the combination of α-viniferin and ε-viniferin in A549 cells led to downregulation of phospho-protein kinase B (p-AKT) and upregulation of cleaved PARP and caspase-3, promoting apoptosis. In vivo experiments using A549 xenograft models further confirmed that ε-viniferin significantly inhibited tumor growth compared to the control, marking it as a potential candidate for cancer therapy.
ε-Viniferin (TV) has been identified as a potent inhibitor of TMEM16A, a calcium-activated chloride channel (CaCC) crucial for intestinal motility. Inhibition of TMEM16A-mediated Cl⁻ currents by TV occurs reversibly, without altering intracellular Ca²⁺ levels or affecting TMEM16A protein expression.
Pharmacological investigations demonstrated that TV effectively suppresses intestinal peristalsis, prolongs gastrointestinal transit time, and reduces spontaneous and stimulated intestinal contractility. Notably, TV exhibited inhibitory effects on contractile responses induced by autonomic stimulation, electromechanical activation (Eact), acetylcholine (ACh), and histamine (HA). These findings suggest that TV could be a valuable agent for treating TMEM16A-associated motility disorders, such as irritable bowel syndrome (IBS) and intestinal hypercontractility.