scholarly journals Branched‐chain amino acids reduce hepatic iron accumulation and oxidative stress in hepatitis C virus polyprotein‐expressing mice

2014 ◽  
Vol 35 (4) ◽  
pp. 1303-1314 ◽  
Author(s):  
Masaaki Korenaga ◽  
Sohji Nishina ◽  
Keiko Korenaga ◽  
Yasuyuki Tomiyama ◽  
Naoko Yoshioka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amino Acids ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Branched Chain Amino Acids ◽  
Iron Accumulation ◽  
Hepatic Iron ◽  
Branched Chain ◽  
Virus Polyprotein ◽  
And Oxidative Stress

Branched-chain amino acids improve insulin resistance in patients with hepatitis C virus-related liver disease: report of two cases

2007 ◽  
Vol 0 (0) ◽  
pp. 070908015728005-??? ◽  
Author(s):  
Takumi Kawaguchi ◽  
Eitaro Taniguchi ◽  
Minoru Itou ◽  
Shuji Sumie ◽  
Tetsuharu Oriishi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Amino Acids ◽  
Hepatitis C Virus ◽  
Liver Disease ◽  
Hepatitis C ◽  
Branched Chain Amino Acids ◽  
Improve Insulin Resistance ◽  
Branched Chain ◽  
Related Liver Disease

Branched chain amino Acids as in vitro and in vivo Anti-Oxidation Compounds

2021 ◽  
pp. 3899-3904
Author(s):  
Moath Alqaraleh ◽  
Violet Kasabri ◽  
Ibrahim Al-Majali ◽  
Nihad Al-Othman ◽  
Nihad Al-Othman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Amino Acids ◽  
Branched Chain Amino Acids ◽  
Raw 264.7 ◽  
Raw 264.7 Cell ◽  
Branched Chain ◽  
Raw 264.7 Cell Line

Background and aims: Branched chain amino acids (BCAAs) can be tightly connected to metabolism syndrome (MetS) which can be counted as a metabolic indicator in the case of insulin resistance (IR). The aim of this study was to assess the potential role of these acids under oxidative stress. Material and Methods: the in vitro antioxidant activity of BCAAs was assessed using free radical 1, 1-diphenyl-2-picryl-hydrazyl (DPPH) scavenging assays. For further check, a qRT-PCR technique was madefor detection the extent of alterations in gene expression of antioxidative enzymes (catalase and glutathione peroxidase (Gpx)) in lipopolysaccharides (LPS(-induced macrophages RAW 264.7 cell line. Additionally, BCAAs antioxidant activity was evaluated based on plasma H2O2 levels and xanthine oxidase (XO) activity in prooxidative LPS-treated mice. Results: Different concentrations of BCAAs affected on DPPH radical scavenging activity but to lesser extent than the ascorbic acid. Besides, BCAAs obviously upregulated the gene expression levels of catalases and Gpx in LPS-modulated macrophage RAW 264.7 cell line. In vivo BCAAs significantly minimized the level of plasma H2O2 as well as the activity of XO activity under oxidative stress. Conclusion: our current findings suggest that BCAAs supplementation may potentially serve as a therapeutic target for treatment of oxidative stress occurs with atherosclerosis, IR-diabetes, MetS and tumorigenesis.

[433] FK506 AMELIORATES METABOLIC DISTURBANCE AND OXIDATIVE STRESS IN HEPATITIS C VIRUS INFECTION

2007 ◽  
Vol 46 ◽  
pp. S165-S166
Author(s):  
K. Moriya ◽  
H. Miyoshi ◽  
S. Shinzawa ◽  
T. Tsutsumi ◽  
H. Fujie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Metabolic Disturbance ◽  
Hepatitis C Virus Infection ◽  
And Oxidative Stress

scholarly journals Arsenic Trioxide Inhibits Hepatitis C Virus RNA Replication through Modulation of the Glutathione Redox System and Oxidative Stress

2008 ◽  
Vol 83 (5) ◽  
pp. 2338-2348 ◽  
Author(s):  
Misao Kuroki ◽  
Yasuo Ariumi ◽  
Masanori Ikeda ◽  
Hiromichi Dansako ◽  
Takaji Wakita ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Arsenic Trioxide ◽  
Redox System ◽  
Rna Replication ◽  
Hcv Rna ◽  
Glutathione Redox System ◽  
And Oxidative Stress ◽  
Glutathione Redox

ABSTRACT Arsenic trioxide (ATO), a therapeutic reagent used for the treatment of acute promyelocytic leukemia, has recently been reported to increase human immunodeficiency virus type 1 infectivity. However, in this study, we have demonstrated that replication of genome-length hepatitis C virus (HCV) RNA (O strain of genotype 1b) was notably inhibited by ATO at submicromolar concentrations without cell toxicity. RNA replication of HCV-JFH1 (genotype 2a) and the release of core protein into the culture supernatants were also inhibited by ATO after the HCV infection. To clarify the mechanism of the anti-HCV activity of ATO, we examined whether or not PML is associated with this anti-HCV activity, since PML is known to be a target of ATO. Interestingly, we observed the cytoplasmic translocation of PML after treatment with ATO. However, ATO still inhibited the HCV RNA replication even in the PML knockdown cells, suggesting that PML is dispensable for the anti-HCV activity of ATO. In contrast, we found that N-acetyl-cysteine, an antioxidant and glutathione precursor, completely and partially eliminated the anti-HCV activity of ATO after 24 h and 72 h of treatment, respectively. In this context, it is worth noting that we found an elevation of intracellular superoxide anion radical, but not hydrogen peroxide, and the depletion of intracellular glutathione in the ATO-treated cells. Taken together, these findings suggest that ATO inhibits the HCV RNA replication through modulation of the glutathione redox system and oxidative stress.

Protective role of amantadine in mitochondrial dysfunction and oxidative stress mediated by hepatitis C virus protein expression

2014 ◽  
Vol 89 (4) ◽  
pp. 545-556 ◽  
Author(s):  
Giovanni Quarato ◽  
Rosella Scrima ◽  
Maria Ripoli ◽  
Francesca Agriesti ◽  
Darius Moradpour ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Protein Expression ◽  
Mitochondrial Dysfunction ◽  
Protective Role ◽  
Virus Protein ◽  
And Oxidative Stress
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