(-)-Epicatechin and related procyanidins modulate intracellular clacium and prevented oxidation in Jurkat T cells

S. V. VERSTRAETEN; G. G. MACKENZIE; C. G. FRAGA; P. I. OTEIZA

Santa Barbara, EEUU

Congreso; Oxygen Club of California 2008 Meeting; 2008

We investigated the effects of (-)-epicatechin (EC), its oligomers, dimer B2 (B2), and trimer C1 (C1), on calcium mobilization and cell oxidation. Jurkat T cells were subjected to a calcium mobilization challenge by replacing Na+ with K+ (K) in the incubation media. A 200 % increase in intracellular calcium concentration ([Ca]i) was observed, and that effect was prevented by the presence of inhibitors of calcium mobilization. The preincubation of the cells in the presence of EC, B2 or C1 prevented K-mediated increase in [Ca]i. IC50 were 10, 24, and 197 nM for EC, B2 and C1, respectively. Cell membrane depolarization was affected by K, but neither inhibitors of calcium mobilization, EC, B2, or C1 modified the increase in membrane potential. A 98 % increase in cell oxidants was observed after cell exposure to K. This increase was prevented by the inhibition of calcium mobilization, NADPH oxidase, and protein kinase C, as well as by 10 nM EC, 10 nM B2, or 100 nM C1. In addition, EC and B2 (100 nM) significantly inhibited the activation of the [Ca]i-regulated transcription factor NFAT. These results indicate that EC and related oligomers, assayed at physiologically achievable concentrations, can modulate [Ca]i and then prevent cell oxidation and other calcium-regulated events.+ with K+ (K) in the incubation media. A 200 % increase in intracellular calcium concentration ([Ca]i) was observed, and that effect was prevented by the presence of inhibitors of calcium mobilization. The preincubation of the cells in the presence of EC, B2 or C1 prevented K-mediated increase in [Ca]i. IC50 were 10, 24, and 197 nM for EC, B2 and C1, respectively. Cell membrane depolarization was affected by K, but neither inhibitors of calcium mobilization, EC, B2, or C1 modified the increase in membrane potential. A 98 % increase in cell oxidants was observed after cell exposure to K. This increase was prevented by the inhibition of calcium mobilization, NADPH oxidase, and protein kinase C, as well as by 10 nM EC, 10 nM B2, or 100 nM C1. In addition, EC and B2 (100 nM) significantly inhibited the activation of the [Ca]i-regulated transcription factor NFAT. These results indicate that EC and related oligomers, assayed at physiologically achievable concentrations, can modulate [Ca]i and then prevent cell oxidation and other calcium-regulated events.i) was observed, and that effect was prevented by the presence of inhibitors of calcium mobilization. The preincubation of the cells in the presence of EC, B2 or C1 prevented K-mediated increase in [Ca]i. IC50 were 10, 24, and 197 nM for EC, B2 and C1, respectively. Cell membrane depolarization was affected by K, but neither inhibitors of calcium mobilization, EC, B2, or C1 modified the increase in membrane potential. A 98 % increase in cell oxidants was observed after cell exposure to K. This increase was prevented by the inhibition of calcium mobilization, NADPH oxidase, and protein kinase C, as well as by 10 nM EC, 10 nM B2, or 100 nM C1. In addition, EC and B2 (100 nM) significantly inhibited the activation of the [Ca]i-regulated transcription factor NFAT. These results indicate that EC and related oligomers, assayed at physiologically achievable concentrations, can modulate [Ca]i and then prevent cell oxidation and other calcium-regulated events.i. IC50 were 10, 24, and 197 nM for EC, B2 and C1, respectively. Cell membrane depolarization was affected by K, but neither inhibitors of calcium mobilization, EC, B2, or C1 modified the increase in membrane potential. A 98 % increase in cell oxidants was observed after cell exposure to K. This increase was prevented by the inhibition of calcium mobilization, NADPH oxidase, and protein kinase C, as well as by 10 nM EC, 10 nM B2, or 100 nM C1. In addition, EC and B2 (100 nM) significantly inhibited the activation of the [Ca]i-regulated transcription factor NFAT. These results indicate that EC and related oligomers, assayed at physiologically achievable concentrations, can modulate [Ca]i and then prevent cell oxidation and other calcium-regulated events.i-regulated transcription factor NFAT. These results indicate that EC and related oligomers, assayed at physiologically achievable concentrations, can modulate [Ca]i and then prevent cell oxidation and other calcium-regulated events.i and then prevent cell oxidation and other calcium-regulated events.