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. 2014 Dec 29;16(1):628–644. doi: 10.3390/ijms16010628

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© 2014 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).

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DSC inhibited H₂O₂-induced mitochondrial membrane potential (ΔΨ_m) loss and apoptosis in HUVEC. HUVEC were incubated with indicated concentrations of DSC or NAC for 4 h, then stimulated with H₂O₂ (200 μM) for 2 or 12 h; the ΔΨ_m (A) and apoptosis (B) were measured by flow cytometry, respectively. Data shown are means ± SEM, ^& p < 0.05 compared with unstimulated cells, * p < 0.05 compared with H₂O₂-stimulated cells. Data were from at least three independent experiments, each performed in duplicate.

DSC inhibited H₂O₂-induced mitochondrial membrane potential (ΔΨ_m) loss and apoptosis in HUVEC. HUVEC were incubated with indicated concentrations of DSC or NAC for 4 h, then stimulated with H₂O₂ (200 μM) for 2 or 12 h; the ΔΨ_m (A) and apoptosis (B) were measured by flow cytometry, respectively. Data shown are means ± SEM, ^& p < 0.05 compared with unstimulated cells, * p < 0.05 compared with H₂O₂-stimulated cells. Data were from at least three independent experiments, each performed in duplicate.