Mitoquine Research Paper

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Mitoquinone (MitoQ) is a highly potent, orally active, mitochondrial targeted coenzyme Q analogue that protects against oxidative damage in a number of in vitro and in vivo systems. Structurally, it consists of a triphenylphosphonium cation and a ubiquinone moiety that is linked via a saturated, aliphatic 10-carbon chain (Figure 1A). The lipophilic cation leads to an extensive accumulation of MitoQ within mitochondria where the ubiquinone is reduced to its active antioxidant ubiquinol form (James et al., 2007). Reactive oxygen species (ROS) are important mediators of liver injury having potential to cause a number of deleterious effects. In the liver, ROS induce parenchymal apoptosis and necrosis, trigger the synthesis of profibrogenic soluble …show more content…

The authors could demonstrate that mitochondrial oxidative stress in CCl4-cirrhotic rat livers is significant higher than in normal control livers and that MitQ dose-dependently decreases mitochondrial oxidative stress in all cell types isolated from cirrhotic rat livers. When PCLS were exposed to MitoQ, the authors found a significant decrease in α-smooth muscle actin (α-SMA), collagen type I α1 (col1α1) and platelet-derived growth factor receptor-β (pdgfrβ) indicating an abrogation of HSC activation. Likewise, the expression of these genes was dose-dependently decreased in primary human HSC, in LX-2 cells, and in HSC that were isolated from CCl4-cirrhotic rats without affecting cell viability. These beneficial effects were corroborated with a significant decrease in mitochondrial oxidative stress formation as demonstrated by staining with a specific fluorescently-labeled mitochondrial superoxide indicator for liver-cell imaging. In addition, MitoQ-treated rats had lower nitrotyrosinated protein quantities and showed decreased expression of …show more content…

In both models, MItoQ hat no impact on mean arterial pressure and hearth rate showing that the compound does not affect systemic hemodynamics. From the therapeutic view, it is most interesting that MitoQ decreased hepatic hydroxyproline content (-20%) and collagen deposition (-68%) in the CCl4 model, the observed alterations were not so pronounced in TAA-treated rats. In both models, the expression of activation markers were decreased in HSC that were isolated from animals subjected to respective treatments. In addition, MitoQ decreased expression of pro-inflammatory markers including TNF-α, iNOS, IL-6 and IL-1β in CCl4-cirrhotic rats and further decreased the number of cells positive for the macrophage lineage indicator

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