We-P14:424 The effect of anthocyanins on oxidative-antioxidative balance hipercholesterolaemic patients

Kopff, Anna; Kowalezyk, E.; Kopff, Maria; Błaszczyk, Jan

doi:10.1016/s1567-5688(06)81777-0

Cited by 1 publication

(2 citation statements)

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“…(43). Results from literature along with our own suggest that ASA could be a good antiviral candidate most probably attributable to its antioxidative and anti-inflammatory properties (21,31,42,43). There are previous reports suggesting antiviral activity of ASA.…”

Section: Discussionmentioning

confidence: 57%

“…Detection of oxidatively damaged proteins was done with an Oxiblot-Oxidative Protein detection kit (Chemicon International, Temecula, CA), according to the manufacturer's recommendation. In addition, the intracellular ROS levels were assessed in total cellular extracts by using the DCF-HDA (Molecular Probes) fluorescence assay, as described previously (21,32). Briefly, after preincubation with above mentioned chemicals, cells were exposed to DCF-HDA (2 mM, in DMSO) for an additional 60 min to detect ROS production.…”

Section: Methodsmentioning

confidence: 99%

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Cu/Zn superoxide dismutase (SOD1) induction is implicated in the antioxidative and antiviral activity of acetylsalicylic acid in HCV-expressing cells

Rivas-Estilla¹,

Bryan-Marrugo²,

Trujillo-Murillo³

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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Rincón-Sánchez AR. Cu/Zn superoxide dismutase (SOD1) induction is implicated in the antioxidative and antiviral activity of acetylsalicylic acid in HCV-expressing cells. Am J Physiol Gastrointest Liver Physiol 302: G1264 -G1273, 2012. First published March 22, 2012 doi:10.1152/ajpgi.00237.2011We evaluated the participation of oxidative stress in the negative regulation of hepatitis C virus (HCV)-RNA induced by acetylsalicylic acid (ASA). We used the HCV subgenomic replicon cell system that stably expresses HCV-nonstructural proteins (Huh7 HCV replicon cells) and the parental cell line. Cells were exposed to 4 mM ASA at different times (12-72 h), and pyrrolidine dithiocarbamate (PDTC) was used as an antioxidant control. Reactive oxygen species (ROS) production, oxidized protein levels, cytosolic superoxide dismutase (Cu/Zn-SOD), and glutathione peroxidase (GPx) activity were measured to evaluate oxidative stress. In addition, viral RNA and prostaglandin (PGE 2) levels were determined. We observed that ASA treatment decreased ROS production and oxidized protein levels in a time-dependent fashion in both parental and HCV replicon cells with a greater extent in the latter. Similar results were found with PDTC exposure. Average GPx activity was decreased, whereas a striking increase was observed in average cytosolic SOD activity at 48 and 72 h in both cells exposed to ASA, compared with untreated cells. HCV replicon cells showed higher levels of Cu/Zn-SOD expression (mRNA and protein) with ASA treatment (48 and 72 h), whereas NS5A protein levels showed decreased expression. In addition, we found that inhibition of SOD1 expression reversed the effect of ASA. Interestingly, PDTC downregulated HCV-RNA expression (55%) and PGE2 (60%) levels, imitating ASA exposure. These results suggest that ASA treatment could reduce cellular oxidative stress markers and modify Cu/Zn-

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